UC  SOUTHERN  REGIONAL  LIBRARY  FACILITY 


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THE  LIBRARY 

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THE  UNIVERSITY 

OF  CALIFORNIA 

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This  book  is  DUE  on  the  last  date  stamped  below 


UNlViiiv  ...u^ORNIA 

LUb  AInGELES 
LIBRARY 


HANDBOOK 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


BY 


JAMES   ROSS,  M.D.,  LL.D., 

FEM.OW   or   THE    ROYAL    roM.EGE    OF    PHYSICIANS    OF    LONDON,    AND    SENIOR    ASSISTANT    PHYSICIAN    TO    THE 
MANCHESTER    ROVAI.    INFIRMARY. 


WITH  ONE  HUNDRED  AND  EIGHTY-FOUR  ILLUSTRATIONS. 


4B  8-^ 


PHILADELPHIA: 

LEA    BROTHERS     &     CO 

1885. 


k 


•3193 


a 


i 


Entered  according  to  the  Act  of  Congress,  in  the  year  1885,  by 

LEA    BEOTHEES    &    CO., 

In  the  Office  of  the  Librarian  of  Congress.     All  rights  reserved. 


7  48 


PHILADELPHIA : 
nORNAK,      PRINTER, 

634  Filbert  Street. 


R73Bh 


PREFACE. 


This  Handbook  is  intended  for  the  use  of  students,  and  such  of 
my  medical  brethren  as  are  so  fully  occupied  in  practice  that  little  time 
is  left  to  them  for  reading  lengthy  treatises,  and  monographs  on  special 
subjects.  The  work  is  divided  into  two  parts — a  general  and  special 
neurology.  In  the  former  I  have  endeavored  to  give  a  brief  outline  of 
the  evolution  and  dissolution  of  nervous  structures  and  functions,  adding 
a  chapter  on  the  general  principles  of  treatment.  In  approaching  a 
new  subject  our  capacity  to  master  it  may  be  measured  by  the  ease  and 
thoroughness  with  Avhich  the  mind  assimilates  with  its  previous  stock  of 
knowledge  the  new  facts  and  relations  presented  to  it.  The  student 
may,  indeed,  acquire  much  information  concerning  diseases  or  any  other 
new  subject  of  study  without  assimilating  the  new  fiicts,  which  come 
under  his  notice,  with  well-established  principles,  but  the  knowledge 
thus  obtained — if  it  deserves  the  name  of  knowledge — is  not  ])roperly 
organized,  and  will  be  found  to  be  both  Meeting  and  ill-adapted  for 
\^  guidance  in  emergencies.  Keeping  these  considerations  in  view,  it  has 
\^  been  my  endeavor  in  this  part  to  arrange  tlie  anatomical  and  physio- 
logical  facts,  with  which  the  student  is  already  more  or  less  familiar,  in 
^  such  a  way  that  his  mind  may  be  prepared  readily  to  comprehend  the 
multiform  phenomena  of  disease,  and  to  associate  them  with  the  funda- 
mental laws  of  development.  In  the  special  part  my  great  aim  has 
been  to  make  the  work  thoroughly  practical.  With  this  A^iew  I  have 
adopted,  as  far  as  possible,  a  clinical  classification,  so  that  the  diseases 
wliich  are  most  apt  to  be  mistaken  for  each  other  will  be  found  described 
in  close  proximity,  and  the  reader  can  thus  note  the  various  features 
which    differentiate    nervous    diseases    clinically    allied.      My    rule   of 


VI  ■  PREFACE. 

selection  lias  been  to  give  the  clinical  descriptions  with  tolerable 
fulness,  and  to  leave  out  the  details  of  morbid  anatomy  and  physiology, 
and  almost  all  reference  to  the  opinions  and  theories  of  different  authori- 
ties. But  although  want  of  space  has  prevented  me  from  quotino- 
authorities,  I  am  none  the  less  grateful  to  men  like  Hughlings-Jackson, 
Wilks,  Terrier,  Charcot,  Westphal,  Leyden,  and  the  other  great  masters 
who  have  placed  our  knowledge  of  nervous  diseases  upon  a  secure  and 
unshakable  foundation. 

JAMES    ROSS. 

Manchester,  November,  1885. 


LIST   OF   ILLUSTRATIONS. 


FIG. 
1. 


9. 
10. 
11. 

12. 
13. 
14. 
15. 
16. 
17. 
18. 

19. 

20. 
21. 

22. 
23. 

24. 
25. 

26. 
27. 

28. 


Diagram    of    the    Distribution   of   the    Bloodvessels,    and    Grouping    of 

Ganglion  Cells  in  the  Spinal  Cord 
Section  of  the   Medulla   Oblongata,   showing    the    Distribution    of  the 
Vessels    ............ 

Diagram  of  the  Distribution  of  the  Vessels  at  the  Base  of  the  Cerebrum 
View  of  the  Brain  from  below    ........ 

Inner  Surface  of  Right  Hemisphere    ....... 

Outer  Surface  of  the  Left  Hemisphere        ..... 

Transverse  Section  of  the  Cerebral  Hemispheres,  about  1  cm.  behind  the 
Optic  Commissure  .... 

Diagram  showing  the  relation  of  the  Spines  of  the  Vertebrae  to  the  Origin 
of  the  Nerves  ......... 

Lateral  View  of  the  Human  Skull     ...... 

Diagram  showing  the  Relations  of  the  Convolutions  to  the  Skull 
Horizontal  Section  of  the  Brain  of  a  Child  nine  months  of  age,  the  righ 

side  being  at  a  somewhat  lower  level  than  the  left  half 
Prefrontal  Section      .... 

Pedunculo-frontal  Section  . 

Frontal  Section   ..... 

Parietal  Section  ..... 

Pedunculo-parietal  Section 
Occipital  Section  .... 

The  Anterior  Surface  of  the  Spinal  Segment,  the   Anterior  Root  of  the 

Right  Side  being  Divided 
Section  from  the  Middle  of  the  Cervical  Enlargement  of  the  Spinal  Cord 

at  the  Third  Month  of  Embryonic  Life 
'I  Sections  of  the  Spinal  Cord  of  a  Five-months'  Human  Embryo,  from  1 
/      Middle  of  the  Cervical  and  Lumbar  Enlargements,  respectively  .       > 
\  Sections  of  Spinal  Cord  of  a  Nine-months'  Human  Embryo,  from  the  ) 
i      Middle  of  the  Lumbar  and  Cervical  Enlargements,  respectively         * 
■)  Sections  of  the  Adult  Spinal  Cord  from  the  Middle  of  the  Lumbar  and  \ 
J      Cervical  Enlargements,  respectively      ......       i 

■)  Sections  of  the  Adult  Human  Spinal  Cord,  from  the  Upper  Cervical  \ 
i      and  Dorsal  Regions,  respectively    .......' 

Section  of  the  Medulla  Oblongata  on  a  level  with  the  Superficial  Origin 
of  the  Acoustic  Nerve    .......... 


22 

23 
25 
27 
28 
29 

30 

32 
33 
35 

37 
38 
39 
39 
40 
40 
41 

41 

42 
42 

43 

43 

44 

46 


viii  LIST    OF    ILLUSTRATIONS. 


FIG. 


PAGE 

29.  Transverse  Section  of  the  Cervical  Part  of  the  Spinal  Cord  of  a  Human 

Embryo  of  Six  Weeks 47 

30.  Transparent  Section  of  a  Furrow  of  the  Third  Cerebral  Convolution  of 

Man 50 

31.  Pyramidal  Giant-cell 51 

32.  Schema  of  the  Cerebro-spinal  System 52 

33.  Schema  of  the  Cerebello-spinal  System 55 

34.  Cord  of  Human  Embryo  at  Five  Months 56 

35.  Diagrammatic  Kepresentation  of  Embryological  Tracts    ....  57 

36.  Diagram  of  the  Gray  Masses  of  the  Spinal  Cord  and  Brain,  showing  the 

course  of  the  Conducting  Paths 59 

37.  Diagram  of  Transverse  Section  of  the  Spinal  Cord  in  upper  half  of  the 

Dorsal  Kegion         ...........  00 

38.  Diagram  of  the  Spinal  Segment  as  a  Centre  and  Conducting  Medium       .  61 

39.  Diagram  of  the  Course  of  the  Principal  Conducting  Paths  within  the  Cord  66 

40.  Upper  Surfoce  of  the  Brain  of  the  Monkey 71 

^2  I  Side  and  upper  Views  of  the  Brain  of  Man I  73 

43.  Schema  of  Encephalo-spinal  Action 76 

44.  Diagram   Illustrating  the  Attachments  of  some  of  the  most  important 

Muscles  which  keep  the  Body  in  the  Erect  Posture       ....       78 

45.  Horizontal    Section  of  the    Basal    Ganglia   and    Internal    Capsule  of   a 

Nine-months'  Embryo    ..........       86 

46.  Transverse  Section  of  the  Crus  Cerebri  on  a  level  with  the  Anterior  Pair 

of  Corpora  Quadrigemina,  from  a  Nine-months'  Embryo      ...       87 

47.  Transverse  Section  of  the  Pons  on  a  level  with  the  Abducens  and  Facial 

Boots,  from  a  Nine-months'  Embryo     .......  88 

48.  Ganglion  Cells  of  the  Anterior  Gray  Horns  of  the  Spinal  Cord        .         .  97 

49.  Alterations  in  Nerve  Fibres  after  Section  .......  98 

f  Transverse  Section  of  the  Spinal  Cord,  from  the  Middle  of  the  Cervi-  ] 

50-    I       cal  Enlargement,  Dorsal  Region  and  Lumbar  Region,  respectively,    I 
rn    ^       showing  Ascending  Degeneration  of  the  Columns  of  Goll,  and  of 
I       the  Direct  Cerebellar  Tract  ....... 

53.  Horizontal  Section  of  the  Right  Hemisphere  Parallel  with  the  Fissure 

of  Sylvius       .         .         .         .         .         .         .         .         .         .         .         .11.5 

54.  Horizontal   Section  of  the  Crura   Cerebri   in  a  case  of  Secondary  De- 

generation      .         .         .         .         .         .         .         .         .         .         .         .116 

Transverse  Section  of  the  Spinal  Cord  from  the  Middle  of  the  Cer-  ] 
vical   Enlargement,  Dorsal  and  Lumbar  Regions,  respectively,    I 
showing    Descending   Sclerosis  of  the  Pyramidal  Tract   in   the    !' 
I       Lateral  Column  Secondary  to  a  Cerebral  Lesion  ... 


114 


58. 


r  Transverse  Sections  of  the  Spinal  Cord,  from  the  Middle  of  the  T 
J       Cervical  Enlargement,  Dorsal  and  Lumbar  Regions,  respectively,   I 

!  showino-    Primnrv  T.ntprnl    ."-ii^lorricic  r\f  tVio    O.^i'A     /-v^    ^inr^r^-r^A.^-.,,-,  *„     C 


gQ*   j       showing  Primary  Lateral  Sclerosis  of  the  Cofd,  or  Secondary  to   f 


a  Lesion  high  up  in  the  Cord  or  Medulla  Oblongata 
61.  Recent   Softening   of   the   Frontal   Lobe,    Island   of  Reil,  and   Middle 

Third  of  the  Lenticular  Nucleus .         .117 


119 

140 

142 

1 

1 

164 

165 

_, 

LIST    OF    ILLUSTK  ATIONS, 


62.  Diagram  of  Lesions  found  in  the  Anterior  Half  of  the  Lenticular  Nucleus, 

Anterior  Segment  of  the  Internal  Capsule,  and  the  Internal  Third  of 

the  Crusta       .         .         .         .         .         .         .         .         .         .         _         .118 

63.  Diagram  of  the  Optic  Thalami,  Tegmentum,  and  Superior  Peduncles  of 

the  Cerebellum        •-........ 

64.  Atrophy  of  Muscular  Fibres  from  a  case  of  Infantile  Paralysis 

65.  Appearance  of  Muscle  in  Infantile  Paralysis      ..... 
66-    f  Diagrams   representing   the    General    Kelations   of    Motor    Power, 
go"  -{       Electrical  Excitability  and  Structural  Changes  of  the  Nerves  and 
gg    I       Muscles  present  in  Different  Stages  of  Paralysis 

70.  Diagram  and  Table  showing  the  Approximate  Eelation  to  the  Spinal 

Nerves  of  the  Various  Sensory  and  Keflex  Functions  of  the  Spinal 

Cord 174 

71.  Diagram  of  the  Keflex  Functions  of  the  Spinal  Cord         ....     180 

72.  Schema  explaining  Conjugate  Deviation  of  the  Eyes  and  Kotation  of  the 

Head  and  Neck 186 

73.  Superior  Cervical    Ganglion  of  the    Sympathetic:    its  Connections    and 

Branches  ............     195 

74.  Nervous  Mechanism  of  the  Iris  .         ........     197 

75.  Schema  of  the  Action  of  the  Cardiac  Nervous  Mechanism         .         .         .     205 

76.  Diagram  showing  the  Probable  Plan  of  the  Centre  for  Micturition  .         .     213 

77.  Sensory  Nerves  of  the  Head  and  Face        .......     246 

78.  Diagram  of  the  First  and  Second  (Superior  Maxillary)  Divisions  of  the 

Fifth  Nerve  :  its  Connections  and  Chief  Branches        ....     248 

79.  Diagram  of  the  Third  (Inferior  Maxillary)  Division  of  the  Fifth  Nerve 

its  Connections  and  Chief  Branches       ...... 


80  "> 

>  Cutaneous  Nerves  of  the  Trunk  ;  Upper  Extremity 


250 
251 


259 
261 

271 

275 


81./ 

82.  Cutaneous  Nerves  of  the  Lower  Extremity         ..... 

83.  Distribution  of  Keddened  Surface  in  Neuralgia  Plantaris  . 

84.  Diagram  of  Glosso-pbaryngeal  Nerve:  its  Connections  and  Branches 

85.  Diagram  showing  the  Fields  of  Color  Vision  in  a  Normal  Emmetropic 

Eye  on  a  Dull  Day 

86.  Horizontal  Section  through  the  Optic  Nerve  at  its  Point  of  Insertion  in 

the  Globe,  and  its  Passage  through  the  Membranes  of  the  Eye 

87.  Diagram  of  Decussation  of  the  Optic  Tracts      .... 

88.  Section  of  the  Medulla  Oblongata  on  a  level  with  the  Largest  Diameter 

of  the  Diseased  Focus,  which  is  represented  by  the  Shaded  Part  on  the 
Left  Half  of  the  Diagram      ...... 

89.  Spasm  of  the  Trapezius       ....... 

90.  Spasm  of  Splenius       ........ 

91.  Contraction  of  the  Khomboid  Muscles        .... 

92.  Position  of  the  Hand  in  Spasm  of  the  Interosseous  Muscles 

93.  Diagram  showing  Position  of  Body  in  Tetanus 

94.  Diagram  showing  Lesion  in  Crural  Monospasms 

95.  Diagram  showing  Lesion  in  Brachial  Monospasm 

96.  Diagram  showing  position  of  Eyeballs  in  a  case  of  Oculo-motor  Mono- 

spasm     .............     326 


280 

284 


285 
308 
305 
306 
308 
316 
324 
325 


X  LIST    OF    ILLUSTRATIONS, 

FIG. 

97.  External  Convex  Surface  of  the  Human  Brain 

98.  Diagram  of  the  First  or  Ophthalmic  Division  of  the  Fifth,  showing  also 

the  Third,  Fourth,  and  Sixth  Cranial  Nerves 
99.1 

.  [: 


360 
867 
372 


374 


100.  [-  Disorders  of  Movements  of  Eyelids 

101.  J 

102.  Kelations  of  the  False  to  the  True  Image 

108.  Diagram  of  the  Facial  Nerve:  its  Connections  and  Branches 

104.  Diagram  of  the  Hj'poglossal  Nerve :  its  Connections  and  Branches 

105.  Diagram  of  the  Pneumogastric  and  Spinal  Accessory  Nerves  :  their  Con 

nections  and  Branches     ......... 

106.  Distortion  of  the  Uvula  in  a  case  of  Peripheral  Paralysis  of  the  Eight 

Side  of  the  Face 

107.  Schema  of  a  Horizontal  Section  through  the  Larynx 

108.  Schema  of  a  Horizontal   Section   through   the    Larynx,    showing   the 

Action  of  the  Arytenoid  Muscles  ...... 

109.  Schema  of  Horizontal  Section   through   the  Larynx,    illustrating   the 

Action  of  Crico-arytenoidei  Laterales  Muscles      .... 

110.  Laryngoscopic  Appearances  of  the  Interior  of  the  Larynx 

111.  Laryngoscopic  Appearance  of  the  Larynx  during  Quiet  Breathing 

112.  The  Laryngoscopic  Appearance  of  the  Larynx  during  Vocalization 

113.  The  Laryngoscopic  Appearance  of  the  Larynx  during  Deep  Inspiration 

showing  the  Bifurcation  of  the  Trachea         ..... 

114.  Nerves  of  the  Cervical  Plexus  ........ 

115.  Nerves  of  the  Brachial  Plexus  .         ....... 

116.  Paralysis  of  the  Serratus  Magnus     ....... 

117.  Distribution  of  the  Sensory  Nerves  on  the  Back  of  the  Hand 

118.  Showing  the  Distribution  of  the  Anaesthesia  in  a  case  of  Division  of  the 

Musculo-spiral  Nerve  in  the  Arm  .'.... 

119.  The  Dorsal  Aspect  of  the  Hand  two  weeks  after  Kesection  of  the  Kadial 

Nerve      ............ 

121   [Cutaneous  Nerves  of  the  Trunk  and  Upper  Extremity  . 

122.  ■)  Pvadial  Border  and  Dorsal  Aspect  of  one  Hand,  showing  the  Distri 
l-^^-  i      bution  of  Aniesihesia  in  a  case  of  Division  of  the  Median  Nerve 

124.  Showing  the  Distribution  of  the  Aniesthesia  on  the  Back  of  the  Fingers 

in  a  case  of  Injury  of  the  Median  Nerve 39-5 

125.  Main  en  GritFe 3<I6 

127!  J  -^^^ion  of  Aniesthesia  in  Paralysis  of  the  Ulnar  Nerve  .         .         .     397 

128.  Attitude  of  the   Hand  in  Pachymeningitis  Cervicalis   Hypertrophica, 

when  the  Disease  is  situated  on  a  Level  with  the  Lower  Half  of  the 
Cervical  Enlargement  of  the  Spinal  Cord 399 

129.  Region  of  Anteslhesia  in  a  case  of  Cervical  Pachymeningitis  . 

130.  Region  of  AnsBsthesia  in  a  case  of  Tubercular  Spinal  Tumor  . 
131  1 
J32;  I  ^distribution  of  Anaesthesia  in  Rupture  of  the  Brachial  Plexus 

133.  Region  Unaffected  by  Rupture  of  the  Brachial  Plexus 

134.  Lumbar  Plexus 

135.  Sacral  and  Coccygeal  Nerves 


PAGE 

348 


357 
3-58 


375 
378 

378 

379 
380 

380 
380 

380 
384 
386 
390 
392 

392 


392 
393 

394 


400 
40O 

401 

401 
404 
406 


LIST    OF    ILLUSTRATIONS.  xi 


PAGE 


13(3.  Cutaneous  Nerves  of  the  Lower  Extremity      ......     410 

137.  Case  of  Infantile  Paralysis  (Genu  RecurvHtum) 432 

138.  Main  en  Griffe 438 

.\^'  > Lesions  in  Acute  Spinal  Atrophic  Paralysis /      ^'3'^ 

141.  Transverse  Section  of  the  Spinal  Cord  and  Medulla  Oblongata  at  dif- 

ferent levels,  from  a  case  of  Chronic  Atrophic  Spinal  Paralysis,  show- 
ing the  Disappearance  of  the  Ganglion  Cells 4.j7 

142.  Transverse  Section  of  the  Spinal  Cord  from  the  Middle  of  the  Cervical 

Enlargement,  from  a  case  of  Syringomyelia,  showing  a  Cavity  behind 
the  Posterior  Commissure,  and  Destruction  of  a  large  portion  of  the 
Ganglion  Cells  of  the  Anterior  Gray  Horns  ......     4.58 

143.  Transverse  Section  of  the  Cervical  Enlargement  of  the  Spinal  Cord, 

showing  a  Central  Cavity  which  has  destroyed  considerable  portions  of 

the  Anterior  Gray  Horns         .........     4.j8 

144.  Transverse  Section  of  the  Cervical  Region  of  the  Spinal  Cord,  from  a 

case  of  Progressive  Muscular  Atrophy  .......     4-59 

145.  Transverse  Section  from   the  Middle  of  the   Cervical  Enlargement  of 

the  Spinal  Cord,  from  an  advanced  case  of  Progressive  Muscular 
Atrophy 460 

146.  Transverse  Section  of  the  Spinal  Cord  from  the  Middle  of  the  Cervical 

Enlargement,  showing  that  the   Central  Column  and  a  large  portion 

of  the  Anterior  Gray  Horns  are  Diseased       .         .         .         .         .         .461 

147.  Portion  of  the  Gray  Substance  on  the  Floor  of  the  Fourth  Ventricle  on 

a  level  with  the  Middle  of  the  Hypoglossal  Nucleus,  from  a  case  of 
Progressive  Muscular  Atrophy  with  Bulbar  Paralysis,  showing  the 
Destruction  of  the  Ganglion  Cells  of  the  Nuclei  of  the  Hypoglossal 
and  Pneumogastric  Nerves     .........     462 

148.  Muscular  Fibres  from  a  case  of  advanced  Infantile  Paralysis  withdrawn 

hy  Leech's  Trocar  ...........     464 

149.  Muscular  Fibres   in  Various  Stages  of   Degeneration,  from  a  case  of 

Pseudo-hypertrofhic  Paralysis        ........     466 

150.  Attitude  of  the  Hand  and  Forearm  in  Amyotrophic  Lateral  Sclerosis    .     475 

151  1 

1  r:,o   f  Spasmodic  Paraplegia  of  Infancj' ■     484 

153.  Transverse  Section  of  the  Medulla  Oblongata  on  a  level  with  the  Middle 

of  the  Nucleus  of  the  Hypoglossal 490 

154.  Horizontal  Section  of  the    Basal   Ganglia  and  Internal  Capsule  in  an 

Embryo  of  Nine  Months 491 

155.  Vertical  Section  of  the  Brain  a  little  behind  the  Knee  of  the  Internal 

Capsule,  showing  the  Effects  of  Rupture  of  the  Lenticulo-striate  Artery     492 

156.  Vertical  Section  of  the  Brain  on  a  level  with  the  Posterior  Part  of  the 

Internal  Capsule,  showing  the  Effects  of  Rupture  on  the  Lenticulo- 
optic  Artery  (Hemianissthesia)        ........     494 

157.  Crura  Cerebri.     Transverse  Section  of  the  Crura  Cerebri  on  a  level  with 

the  Anterior  Pair  of  the  Corpora  Quadrigemina,  from  a  Nine-months' 
Human  Embryo      ...........     495 

158.  Diagram  showing  Decussation  of  Fibres  of  Pyramidal   Tract  at   the 

Middle  of  the  Pons 496 


Xll 


LIST    OF    ILLUSTRATIONS. 


159. 

160. 
161. 
162. 
163. 
164. 
165. 
166. 
167. 
168. 

169. 
170. 
171. 
172. 
173. 

174. 

175. 


176. 
177. 

178. 
179. 
180. 

181. 


182. 
183. 
184. 


Dia:;rftni  of  Defect  of  Parietal  Bone  in  a  case  of  Congenital  Paren- 
cephalus .......... 

Appearance  of  Brain  in  a  case  of  Congenital  Parencephalus 

i  Diagram  of  Lesion  in  Crural  Monoplegia 

Diagram  of  Lesion  in  Brachio-crural  Monoplegia    . 
Diagram  of  Lesion  in  Brachio-facial  Monoplegia     . 
Diagram  of  Lesion  in  Facial  Monoplegia 
Diagram  of  Lesion  in  Unilateral  Oculo-motor  Monoplegis 

[-Diagram  of  Lesion  in  Hemiplegia  from  Cortical  Disease 

Transverse  Section  of  the  Lumbar  Region,  from  a  case  of  Locomotor 

Ataxia,  complicated  with  Muscular  Atrophy 

Region  of  Anaesthesia  in  a  case  of  Hemorrhage  into  the  Upper  Dorsal 

Region  of  the  Right  Side  of  the  Cord 

Diagram  of  the  Cutaneous  Symptoms  in  Unilateral  Lesion  of  the  Dorsal 

Portion  of  the  Spinal  Cord  on  the  Left  Side  ...... 

Section  of  the  Middle  of  the  Cervical  Enlargement  of  the  Spinal  Cord 

from  a  case  of  Central  Myelitis      ........ 

Diagram  of  the  Course  of  the  Principal  Conducting  Paths  within  the 

Cord 

Distribution  of  Aniesthesia  in  Pacliymeningitis  Cervicalis  Hypertrophica 
Attitude  of  the   Hand  in    Pachymeningitis  Cervicalis   Hypertrophica, 

when  the  Lesion  is  situated  on  a  level  with  the  Upper  Half  of  the 

Cervical  Enlargement     .......... 

Diagram  of  Lesion  in  a  ca.se  of  Aphasia  ....... 

Diagram   showing   the   Area  of  Distribution  of  the   Middle   Cerebral 

Artery     ............. 

Diagram  of  Lesion  in  a  case  of  Word-deafness         ..... 

Attitude  of  the  Hand  in  Paralysis  Agitans       ...... 

Attitude  of  the  Hand  in  Paralysis  Agitans  simulating  that  of  Arthritis 

Deformans       ............ 

Section  of  Anterior  Gray  Horn  of  the  Cervical   Enlargement  of  the 

Spinal  Cord,  from  a  case  of  Chorea  that  died  on  the  Fourth  Day  of 

Scarlet  Fever  ............ 

Section  of  the  Cervical  Region  of  the  Spinal  Cord,  from  a  case  of  Chorea 

View  of  the  Posterior  Surface  of  the  Medulla 

Transparent  Lateral  View  of  the  Medulla 


498 
499 
500 
501 
501 
502 
503 
505 
505 
506 

532 

544 

559 

563 

566 
572 


573 
644 

645 
646 
672 

673 


684 
685 
697 
698 


CONTENTS. 


CHAPTER   I. 

ANATOMICAL  INTRODUCTION. 


Formation  of  Nervous  Constituknts 
Formation  of  Nervous  Tissues  . 
Formation  of  a  Nervous  System 
Encephalo-spino-neural  System 


■  PACK 

18 
19 
19 
21 


CHAPTER    II. 

PHYSIOLOGICAL   INTRODUCTION. 

1.  Functions  of  the  Spino-neural  System 65 

2.  Functions  of  the  Encephalo-spinal  System 67 

3.  Functions  of  the  Cerebro-spinal  System 68 

4.  Functions  of  the  Cerebello-spinal  System 75 

5.  Cooperation    of     the     Cerebro-spinal    and    Cerebello-spinal 

Systems 76 


CHAPTER    III. 

GENERAL   MORBID   ANATOMY   AND    PHYSIOLOGY   OF   THE 
NERVOUS   SYSTEM. 

I.  General  Morbid  Anatomy   .........  90 

1.  Defects  of  Development         .........  90 

2.  Dissolution  of  the  Nervous  System         .......  93 

3.  Dissolution  of  the  Nervous  System  (continued) 108 

II.  General  Morbid  Anatomy  and  Physiology 122 


CHAPTER    IV. 

GENERAL   SYMPTOMATOLOGY. 

A.  The  .^Esthesioneuroses  ...... 

I.  The  Primary  ^Esthesioneuroses  .... 

II.  The  Secondary  or  Compound  .^Esthesioneuroses 


125 
125 

135 


XIV 


CONTENTS. 


CHAPTEK    V. 

GENERAL   SYMPTOMATOLOGY   {continued) 

B.  Tkoi'iioneurosks 

I.  Neurotic  Atrophy  of  Muscle    . 
II.  Cutaneous  Trophic  Affections  . 

III.  Trophic  Disorders  of  the  Nails  and  Hair 

IV.  Bedsores  and  other  Destructive  Processes 
V.  Nutritive  Affections  of  the  Joints,  Bones,  and  Teeth   (Articular 

and  Osseous  Trophoneuroses)        ...... 

VI.  Nutritive  and  Secretory  Affections  of  the  Glandular  Apparatus 
VII.  Nutritive  Affections  of  the  Viscera  (Visceral  Trophoneuroses) 


PAOE 

140 
140 
143 
145 
146 

151 
15.3 
1.56 


CHAPTER    yi. 

GENERAL   SY:MPT0MAT0L0GY'  (continued). 
C.  The  Elementary  Kinesioneuroses 158 


T.  The  External  Kinesioneuroses 


158 


CHAPTER    VII. 

GENEPvAL   SY'MPTOMATOLOGY  {continued). 
C.  The  Elementary  Kinesioneuroses  {continued)    . 

II.  The  Visceral  Kinesioneuroses    ...... 

III.  Vascular  Kinesioneuroses  or  Angioneuroses 

CHAPTER    VIII. 

GENERAL   TREATMENT 

1.  Prophylactic  Treatment 

2.  Removal  of  the  Exciting  Cause  . 

3.  Removal  of  the  Anatomical  Cause     . 

(a)  Internal  Remedies        .... 
{b)  External  Remedies        .... 

4.  To  Allay  or  Remove  Serious  Symptoms 


194 
194 
21() 


222 
223 
223 
223 
225 
234 


SPECIAL  PATHOLOGY  OF  THE  NERVOUS  SYSTEM. 


CHAPTER    I. 

GENERAL   DISEASES   OF   THE   PERIPHERAL   NERVES. 

1.  Hyper.emia  or  Congestion  of  the  Nerves 237 

2.  Inflammation  of  Nerves  (Neuritis  and  Perineuritis)  .        .        .  237 
o.   Atrophy  of  Nerves 239 

4.  Hypertrophy  of  Nerves 240 

5.  Nkuromata         .  „.„ 

240 


CONTEXTS.  XV 

CHAPTER    II. 

DISORDERS   OF    COMMON   SENSATION   AND   OF    SPECIAL    SENSE. 

PAGE 

I.  Anaesthesia  and  Analgesia  in  thk   Region  of  Distribution  of 

Individual  Nerves  and  Plexuses 243 

II.  Hyper.esthesia  and  Hyperalgesia  in  the  Region  of  Distribu- 
tion of  Individual  Nerves  and  Plexuses          ....  244 

III.  Neuralgia  in  the  Region  of  Distribution  of  Individual  Nerves 

AND  Plexuses     . 24") 

1.  Neuralgia  of  the  Fifth  Nerve  (Trigeminal  Neuralgia)         .         .  24') 

2.  Cervico-occipital  Neuralgia  .........  2-")2 

3.  Phrenic  Neuralgia 252 

4.  Cervico-brachial  Neuralgia    ........  253 

5.  Dorso-intercostal  Neuralgia  .         .                           .....  254 

6.  Lumbar  Neuralgia 255 

7.  Neuralgia  of  the  Sacral  and  Coccygeal  Nerves      ...  257 

8.  Visceral  Neuralgia         ..........  2()2 

IV.  Disorders  of  the  Nerves  of  Si'f.cial  Skxse 2G7 

1.  Diseases  of  the  Olfactory  Nerve 2G7 

2.  Diseases  of  the  Acoustic  Nerves    ...                  ....  269 

3.  Diseases  of  the  Gustatory  Nerves                              270 

4.  Diseases  of  the  Optic  Nerves 273 

V.  Disorders  Caused  by  Disease  of   the   Cerebro-Spinal   Sensory 

Conducting  Paths 284 

VI.  Disorders  Caused  by  Disease  of  the  Cortical  Sensory  Centres.  288 

1.  Cutaneous  and  Muscular  Hemiantcsthesia 288 

2.  Disorders  of  the  Sense  of  Smell     .....•■■  288 

3.  Disorders  of  the  Auditory  Sense 289 

4.  Disorders  of  the  Visual  Sense -Bft 


CHAPTER    III. 


SPASMODIC    DISORDERS 


I.  Spino-neural  Spasms 

1.  Local  Spasms 

2.  General  Spino-neural  Spasms 

3.  Myopathic  Spasms 


CHAPTER    IV. 

SPASMODIC    DISORDERS  {coniinned). 


295 
295 
313 
321 


323 


II.  Cerebro-spinal  Spasms 

1.  Spasms  from  Organic  Disease  of  the  Cortex  of  the  Brain  (Monospa.sms 

and  Unilateral  Convulsions) '^23 

2.  Spasmodic  Atfections  from  Functional  Disease  of  the  Cortex  of  the 

Brain  .....•••■••• 


327 


CONTENTS. 


CHAPTER    V. 

ATROPHIC    PARALYSES. 


Simple  Nkural  Paralyses 

1.  Paralysis  of  the  Oculo-motor  Nerves 

2.  Masticatory  Paralysis 

3.  Paralysis  in  the  Area  of  Distribution  of  the  Seventh  Nerve  (Mimetic 

Paralysis,  Hemiplegia  and  Diplegia  Facialis,  Prosopalgia,    Bell's 
Paralysis)  ....••••••• 

4.  Paralysis  of  the  Muscles  Supplied  by  the  Hypoglossal  Nerve  (Glosso 

plegia) 

5.  Paralysis  of  the  Pneumogastric  Nerve 
(j.  Paralysis  of  the  Spinal  Accessory  Nerve     . 

7.  Paralysis  of  the  Muscles  Supplied  by  the  Cervical  Plexus 

8.  Paralysis  of  the  Muscles  Supplied  by  the  Brachial  Plexus 

9.  Paralysis  of  the  Muscles  Supplied  by  the  Dorsal  Nerves 

10.  Paralysis  of  the  Muscles  Supplied  by  the  Lumbar  Plexus 

11.  Paralysis  of  the  Muscles  Supplied  by  the  Sacral  Plexus 


PAGE 

356 
356 
363 


365 

371 
373 
383 
385 
389 
402 
403 
408 


CHAPTER    VI. 

ATROPHIC   PARALYSES  {continued). 

II.  Multiple  Neural  Paralyses     . 

1.  Idiopathic  Progressive  Multiple  Neuritis 

2.  Lead  Paralysis       ..... 

3.  Alcoholic  Paralysis        .... 

4.  Diphtheritic  Paralysis  .... 
III.  Reflex  Atrophic  Paralyses 


412 
412 
413 
415 
418 
422 


CHAPTER    VII. 

ATROPHIC   PARALYSES  {continued). 

lY.  Spinal  Atrophic  Paraly'ses  (Poliomyelopathies)  .         .         .     425 

1.  Paralysis    Ascendans    Acuta   (Acute   Ascending    Paralysis,  Landry's 

Paralysis)  ............     425 

2.  Poliomyelitis  Anterior  Acuta  (Kussmaul)  (Acute  Inflammation  of  the 

Anterior  Gray  Horns,  Acute  Atrophic  Spinal  Paralysis)  .         .  426 

3.  Poliomyelitis  Anterior  Chronica  (Chronic  Atrophic  Spinal  Paralysis)  434 

4.  Periependymal  Myelitis  (Syringomyelia,  Hydromyelia)        .         .         .  436 

5.  Progressive  Muscular  Atrophy 437 

6.  Primary  Labio-glosso-laryngeal  Paralysis  (Chronic  Progressive  Bulbar 

Paralysis  (Wachsmuth)) 442 

7.  Ophthalmoplegia  Externa  vel  Progressiva 447 

V.  Myopathic  Atrophic  Paralysis 448 

Pseudo-hypertrophic  Paralysis  and   Erb's  Juvenile  Form  of  Progressive 

Muscular  Atrophy 448 

Morbid  Anatomy  and  Physiology  of  the  Atrophic  Paralyses    .         .         .     4-54 


CONTENTS.  xvii 

CHAPTER    VIII. 

THE   SPASMODIC   PARALYSES. 


I'AOE 


I.  Paraplkgi^e 471 

1.  Primary  Lateral  Sclerosis  (Tabes  Dorsalis  Spasinodica  (Charcot),  Spas- 

modic Spinal  Paralysis)     .         .         .         .         .         .         .         .         .471 

2.  Amyotrophic  Lateral  Sclerosis       ........  474 

3.  Secondary  Lateral  Sclerosis  .........  470 

II.  Hemiplegia: 476 

L  Ordinary  Hemiplegia     ..........  470 

2.  Hemiplegia  and  Hemiansesthesiu  ........  477 

3.  Hemiplegia,  Heinianuesthesia,  and  Hemianopsia   .....  477 

4.  Crossed  Hemiplegia        .         .         .                  .•       .                  .         .         .  477 

5.  Hemiplegia  and  Post-hemiplegic  Spasms      ......  478 

III.  Special  Consideration  of  Post-hemiplegic  Spasms  as  they  occur 

IN  Infancy  (the  Spasmodic  Paralyses  of  Infancy)       .        .  482 

1.  Spastic  Hemiplegiae  of  Infancy 482 

2.  The  Spasmodic  Paraplegiije  of  Infancy           ......  484 

IV.  Monoplegia 485 

V.  Paralyses  from  Functional  Disease        ......  485 

1.  Post-epileptic  Paralysis          .........  485 

2.  Hysterical  Paralysis •         .         .  486 

3.  Toxic  Paralyses 488 

Morbid  Anatomy 489 

I.  Paraplegia 489 

II.  Hemiplegia         ...........  491 

III.  Special  Consideration  of  Lesions  of  the  Pyramidal  Tracts  as  they 

occur  in  Infants      ..........  497 

IV.  Monoplegia 499 

CHAPTER    IX. 

DISORDERS   OP    MOTOR   COORDINATION. 

1.  Meniere's  Disease  (Aural  or  Labyrinthine  Vertigo)    .         .        .  509 

2.  Primary  Sclerosis  of  the  Columns  of  Goll 510 

3.  Secondary  Sclerosis  of  the  Columns  of  Goll  and  of  the  Direct 

Cerebellar  Tracts 511 

4.  Progressive  Locomotor  Ataxia  (Tabes  Dorsalis,  Gray  Degenera- 

tion or  Sclerosis  of   the   Posterior   Columns  of  the  Spinal 

Cord) 511 

(1)  The  Preataxic  Stage 512 

(2)  The  Ataxic  Stage 521 

(8)  The  Paralytic  Stage 526 

5.  Combined  Sclerosis  of  the  Posterior  ajsd  Lateral  Columns        .  528 

6.  Diseases  of  the  Cerebellum 528 


PAGE 


CONTENTS, 


CHAPTER    X. 

VASCULAR   DISEASES   OF   THE   SPINAL   CORD. 

I.  Anemia,  Thrombosis,  and  Embolism  of  the  Spinal  Cord  (Myelo- 

malacia, Vascular  Spinal  Sclerosis) 539 

II.    HYPERiEMIA    and    HEMORRHAGE    OF   THE    SPINAL    CORD             .            .            .  540 

L  Spinal  Uyperaemia 540 

2.  Spinal  Apoplexy  (Hajmatorayelia) 541 

CHAPTER    XI. 

MYELITIS. 

Varieties  of  Diffused  Myelitis 551 

1.  Central  Myelitis 551 

2.  Bulbar  Myelitis •         .552 

3.  Transverse  Myelitis 552 

4.  Wounds  of  the  Spinal  Cord 554 

5.  Compression  Myelitis  (Tumors  in  the  Vertebral  Canal)        .         .         .  556 

6.  Spinal    Hemiplegia   and   Hemiparaplegia   (Unilateral  Lesion  of  the 

Spinal  Cord) 557 

7.  Meningo-myelitis  ...........  500 

8.  Universal  Progressive  Myelitis 560 

9.  Disseminated  Myelitis   ..........  561 

CHAPTER    XII. 

DISEASES   OF   THE   SPINAL   MEMBRANES. 

I.  Vascular  Diseases  of  the  Spinal  Membranes       ....  569 

1.  Hj'peraemia    .........'...  569 

2.  Hajmatorrhachis  (Meningeal  Apoplexy)        ......  569 

II.  Inflammation   of  the  Spinal  Dura   Mater   (Pachymeningitis 

Spinalis,  Perimeningitis) 570 

1.  Pachymeningitis  Spinalis  Externa  (Peripachymeningitis)    .          .          .  570 

2.  Pachymeningitis  Interna .         .         .571 

III.  Inflammation  of  the  Spinal  Pia  Mater  and  Arachnoid  (Lepto- 
meningitis Spinalis;    Perimyelitis  and  Arachnitis)           .         .  574 

1.  Leptomeningitis  Spinalis  Acuta    ........  574 

2.  Leptomeningitis  Spinalis  Chronica        .......  575 

CHAPTER    XIII. 

CERTAIN    FUNCTIONAL   DISEASES   OF   THE    NERVOUS   SYSTEM. 

1.  Spinal  Irritation 578 

IL  Neurasthenia 579 

III.  Headache  (Cephalalgia) 584 

Hemicrania 586 


CONTENTS. 


XIX 


CHAPTER    XIY. 

saocK,  coxcussioisr,  and  allied  conditions. 


I.  Shock . 

II.  Concussion  of  the  Spinal  Cord  (Commotio  Spinalis) 
Varieties  of  Spinal  Concussion  ..... 

III.  Concussion  of  the  Brain 

IV.  Contusion  of  the  Brain      ...... 

V.  Compression  of  the  Brain 


PAGE 

594 
596 
596 
598 
599 
600 


CHAPTER    XY. 

VASCULAE   DISEASES   OF   THE    BRAIN. 

I.  Anemia  and  Occlusion  of  the  Intracranial  Vessels        .        .  603 

1.  Universal  Cerebral  Anaemia  ........  603 

2.  Partial  Cerebral  Anemia  (Occlusion  of  the  Intracranial  Ves«els  .  604 

II.  C0NGE.ST10N  of  the  Brain 608 

III.  Intracranial  Hemorrhage 610 

1.  Cerebral  Hemorrhage  (Apoplexy)         .......     610 

2.  Meningeal  Hemorrhage         .........     615 

CHAPTER    XYI. 

ENCEPHALITIS. 

Diffused  or  General  Encephalitis 620 

Partial  or  Local  Encephalitis 620 

1.  Poliencephalitis  Acuta  Infantium  .......  621 

2.  Traumatic  Local  Encephalitis        ........  621 

3.  Acute  Pyiemic  Encephalitis  ........  622 

4.  Encephalitis  Complicating  Preexisting  Lesions  of  the  Brain        .         .  623 

CHAPTER    XVII. 

ATROPHY,   HYPERTROPHY,  AND   TUMORS   OF   THE    BRAIN. 

I.  Atrophy  of  the  Brain 630 

1.  Atrophy  of  the  Corpus  Callosum           .......  630 

2.  Atrophy  of  the  Cerebellum            ........  630 

3.  Atrophy  of  the  Cerebral  Hemispheres           ......  630 

II.  Hypertrophy  of  the  Brain 631 

1.  General  Hypertrophy  of  the  Brain         .......  631 

2.  Partial  Hypertrophy  or  Heterotopia  of  the  Brain  Substance         .         .  631 

III.  Intracranial  Tumors 632 

CHAPTER    XYIII. 

APHASIA. 

Motor  Aphasia 

Sensory  Aphasia  (Amnesic  Aphasia) 

Mixed  Motor  and  Sensory  Aphasia        .... 


638 
640 
643 


CONTENTS. 

CHAPTER    XIX. 

DISEASES   OF   THE   MEMBRANES   OF    THE    BRAIN. 


PAGE 


I.  DrSKASES  OF  THE  DuRA   Mater 651 

(I.)  External  Pachymeningitis 651 

(II.)  Internal  Heniorrnagic   Pachymeningitis  (Hjematoma  of  the  Dura 

Mater) 651 

II.  Diseases  of  the  Pia  Mater. 653 

(I.)  Tubercular  Meniningitis  (Acute  HydrocephHliisj    ....  653 

Chronic  Hydrocephalus   .........  658 

(II.)  Meningitis  of  the  Convexity  of  the  Brain 660 

(III.)  Simple  Meningitis  of  the  Base  of  the  Brain  (Basilar  Meningitis)  663 

(IV.)  Metastatic  Meningitis 664 

(V.)  Traumatic  Meningitis 665 

CHAPTER    XX. 

PAPvALYSIS   AGITANS,  MULTIPLE    SCLEROSIS,  AND   CHOREA. 

I.  Paralysis  Agitans 670 

II.  Multiple  Sclerosis  of  the   Brain  and  Spinal  Cord  (Dissemi- 

nated OR  Insular  Sclerosis) 674 

III.  Chorea 679 

CHAPTER    XXI. 

GENERAL   DIAGNOSIS. 

1.  Clinical  Diagnosis 690 

2.  Topographical  Diagnosis 691 

3.  Pathological  Diagnosis 699 

Syphilis  of  the  Brain  ...  .  ....  705 


DISEASES  OF  THE  NERVOUS  SYSTEM. 


/4387 
CHAPTEK  J. 

ANATOMICAL  INTRODUCTION. 

Before  entering  upon  the  study  of  the  nervous  system  it  is  desirable 
to  lay  down  a  foAV  general  principles,  to  which  all  nervous  structures, 
with  their  corresponding  functions,  must  conform.  The  key  to  the 
interpretation  of  the  form  assumed  by  the  constituent  parts  of  the  ner- 
vous SA'Stem,  and  of  the  actions  performed  by  each  part,  is  best  obtained 
by  a  close  study  of  the  order  of  development  of  nervous  structures  and 
functions  as  manifested  in  passing  from  the  lower  to  the  higher  animals, 
and  from  the  initial  to  the  adult  stages  of  animals.  The  knowledge 
obtained  by  these  studies  constitutes  the  comparative  anatomy  and  em- 
bryology of  the  nervous  system.  The  great  law  to  Avhich  all  developing 
organisms  and  organs,  as  well  as  all  developing  functions,  must  conform 
is  the  law  of  evolution.  This  law  may  be  defined  as  a  progressive 
integration  of  structure  and  function,  during  which  there  is  a  passage 
from  the  uniform  to  the  multiform,  from  the  simple  to  the  complex,  and 
from  the  general  to  the  special. 

In  the  lowest  organisms,  which  consist  of  individual  cells,  or  of  an 
aggregation  of  cells  without  definite  parts,  each  part  performs  all  the 
vital  functions.  Each  part  possesses  the  fundamental  property  of  irrita- 
bility, and  is  capable  of  initiating  movement,  or,  in  other  words,  is 
automatic  and  contractile,  and  each  is  likewise  metabolic,  excretory,  and 
reproductive.  But  on  ascending  in  the  scale  of  organization  it  is  found 
that  certain  parts  of  the  organism  acijuire  the  power  of  performing 
more  perfectly  a  few  functions,  and  ultimately  one  special  function, 
while  losing  to  a  greater  or  less  extent  the  power  of  performing  the 
general  functions.  One  part  or  tissue,  for  example,  becomes  adapted 
to  the  performance  of  the  functions  of  contraction,  while  at  the  same 
time  it  gives  up  the  functions  of  initiating  movement  and  reproduction. 


18  ANATOMICAL  INTRODUCTION. 

and  only  performs  the  metabolic  and  excretory  functions  in  a  very  subor- 
dinate degree.  This  process  has  been  named  a  "  physiological  division 
of  labor,"  or  a  "specialization  of  function,"  when  regarded  from  the 
point  of  view  of  the  actions  of  the  organism,  and  its  anatomical  counter- 
part in  development  is  to  be  found  in  what  is  known  as  the  "differen- 
tiation of  structure." 

FORMATION  OF  NERVOUS  CONSTITUENTS. 

The  first  beo-inning  of  a  differentiation  of  the  nervous  from  the  other 
elements  of  organisms  is  well  illustrated  in  Hydra.  In  this  organism 
the  internal  end  of  an  ectodermic  cell  is  prolonged  into  a  process, 
which,  being  shielded  from  external  influences,  tends  only  to  contract 
when  it  receives  a  stimulus  through  the  external  end.  In  other  words, 
the  internal  end  performs  the  work,  and  the  external  determines  when 
the  work  shall  be  done :  the  one  is  operative,  the  other  regulative. 
This  differentiation  of  structure  is  carried  still  further  in  Beroe,  where 
the  internal  and  external  ends  of  the  ectodermic  cells  are  represented 
by  two  different  cells  connected  by  a  thin  fibre.  The  changes  set  up 
in  the  external  or  sensitive  cell  are  conducted  through  the  fibre  to  the 
internal  cell,  which  it  excites  to  contract.  This  new  arrangement  of 
fibre  introduces  us  to  a  new  specialization  of  function.  The  regulative 
or  automatic  cell  and  the  work  cell  are  separated  from  each  other  by  a 
considerable  distance,  but  the  molar  contraction  of  the  one  is  coordinate 
with  the  molecular  motion  of  the  other  by  the  internuneial  function  of 
the  fibre.  The  property  the  fibre  possesses  of  transmitting  the  state  of 
activity  from  one  end  to  the  other  is  called  its  conductivity. 

The  next  step  in  development  consists  in  the  differentiation  of  the 
external  or  sensitive  cell  into  two  :  one  of  which  becomes  adapted  to 
responding  to  external  stimulation  alone,  and  the  other  to  modifying 
the  impulses  which  are  sent  to  it  from  the  external  cell  and  trans- 
mitting them  to  the  work  cell.  The  nervous  mechanism  now  consists 
of  an  external  sensory  cell,  an  afferent  fibre  connecting  it  with  a  cen- 
tral regulating  cell,  and  an  efferent  fibre  or  fibres  connecting  this  last 
with  work  cells.  This  mechanism  constitutes  a  rejiex  loop,  and  its 
function  is  named  rejiex  action.  One  other  complication  of  this  simple 
mechanism  may  be  mentioned :  When  an  automatic  or  reflex  cell  is 
already  engaged  in  action,  a  new  stimulus  brought  to  it  by  means  of  a 
second  afferent  fibre  may  check,  instead  of  still  further  exciting  that 
action,  so  that  this  function  introduces  us  to  inhibitory  as  well  as  excito- 
motor  fibres.  The  inhibitory  fibres  are  either  afferent,  or  connect  one 
central  cell  with  another  central  cell,  being  then  intercentral,  and  prob- 
ably never  connect  a  central  cell  directly  with  a  work  cell. 


FORMATION    OF    A    NERVOUS    SYSTEM.  19 

FOKMATION  OF  NEEVOUS  TISSUES. 

On  looking  at  a  simple  nervous  system,  the  greatest  contrast  in 
structure  is  manifested  between  certain  knots  termed  ganglia  and 
certain  cords  termed  nerves,  and,  since  these  parts  exhibit  the  greatest 
structural  contrast  existing  in  the  nervous  system,  they  may  also  be 
expected  to  exhibit  the  widest  functional  contrast.  The  ganglia  are 
composed  of  nerve  cells,  with  their  connecting  processes,  held  together 
by  a  fine  connective  tissue ;  and  the  nerves  are  composed  of  nerve  fibres 
arranged  side  by  side  in  a  bundle — these  being  also  held  together  by  a 
firm  connective  tissue  and  by  a  fibrous  sheath. 

Functionally  regarded,  the  ganglia  are  originators  of  motion,  and,  to 
some  extent,  conductors  also ;  while  the  nerves  are  mainly  conductors, 
although  it  is  probable  that  they  are  also  in  some  small  degree  origin- 
ators of  motion.  A  still  further  examination  shows  that  the  afferent 
fibres  are  provided  Avith  peripheral  end-organs,  which  are  adapted  for 
receiving  impressions  from  environing  agents  and  objects ;  while  the 
efferent  fibres  are  provided  with  arrangements  by  means  of  which  the 
molecular  motion  of  the  nervous  system  is  transmitted  into  the  molar 
motion  of  the  work  organs. 

FOKMATION  OF  A  NERYOUS  SYSTEM. 

It  has  just  been  seen  how  the  cells  and  fibres  which  constitute  the 
nerve  elements  integrate  so  as  to  form  the  simple  tissues,  and  now  we 
must  follow  this  progressive  integration  to  still  higher  stages.  In  the 
higher  animals,  the  ganglia,  instead  of  appearing  as  small  knots,  have 
come,  by  approximation  and  fusion,  to  form  a  continuous  mass,  which, 
from  its  color,  is  termed  the  gray  substance;  and  the  fibres,  instead  of 
always  appearing  as  cords  connecting  separate  ganglia,  also  form  a  con- 
tinuous mass  called  the  white  substance.  Now,  this  fusion  of  nerve 
centres  and  nerve  strands  takes  place  when  the  functions  are  integrated 
in  corresponding  degree,  and  fails  to  take  place  when  the  functions 
remain  in  large  measure  independent  of  one  another. 

The  internal  organs  of  the  body  which  are  derived  from  the  hypo- 
blast of  the  embryo  are  much  more  independent  of  one  another  in 
their  actions  than  are  the  external  organs  derived  from  the  epiblast ; 
and  the  functions  of  the  former  are  regulated  chiefly  by  means  of  the 
ganglia  of  the  sympathetic  system,  which  are  only  connected  by  small 
cords,  while  those  of  the  latter  are  regulated  by  means  of  large  masses 
of  gray  and  white  substance,  which  constitute  the  encephalo-spino- 
neural  system. 


20  ANATOMICAL  INTEODUCTION. 

■  The  parts  of  tlie  body  which  are  derived  from  the  mesoblast  form  a 
system  of  organs  which  serve  to  connect  the  external  and  internal 
or<^ans ;  and  fn  so  far  as  the  intermediate  tissues  subserve  the  functions 
of ''the  external  organs  their  actions  are  regulated  from  the  encephalo- 
spinal  and  the  spino-neural  centres ;  and  when  they  subserve  the  func- 
tions of  the  internal  organs  their  actions  are  regulated  by  the  sympa- 
thetic system ;  while  in  so  far  as  their  function  is  intermediate  between 
the  internal  and  external  organs,  but  partially  independent  of  them, 
their  actions  are  regulated  by  an  intermediate  and  partially  inde- 
pendent system,  termed  the  vaso-motor. 

A  plane  passing  longitudinally  and  from  behind  forwards  through  a 
human  being  bisects  the  body  into  two  bilaterally  symmetrical  divisions, 
and  this  statement  is  equally  true  of  the  nervous  system  as  of  the  body 
as  a  whole.  The  sympathetic  system  of  each  half  of  the  body  is  rep- 
resented by  a  gangliated  cord,  which  is  situated  along  the  side  of  the 
vertebral  column ;  while  the  encephalic  and  spinal  systems  of  each  side 
are  represented  by  the  cerebral  and  cerebellar  hemispheres,  the  crus 
cerebri,  and  the  lateral  halves  of  the  pons,  medulla  oblongata,  and  spinal 
cord.  Although  the  two  lateral  halves  of  the  body  are  more  or  less 
symmetrical,  the  organs  of  the  one  side  are  to  a  considerable  extent 
dependent  upon  those  of  the  other  in  their  functions,  and  consequently 
the  actions  of  the  organs  of  the  two  sides  must  be  duly  coordinated. 
The  structural  counterpart  of  this  interdependence  is  to  be  found,  in 
the  case  of  the  sympathetic  system,  in  the  plexus  of  fibres  and  small 
ganglia  which  pass  in  front  of  the  vertebral  column  and  connect  the 
ganghated  cords  of  the  two  sides  with  one  another ;  and  in  the  en- 
cephalic and  spinal  systems  by  the  commissures  of  the  spinal  cord,  the 
median  raphe  of  the  medulla  oblongata  and  pons,  the  middle  peduncles 
of  the  cerebellum,  the  commissures  of  the  third  ventricle,  and  the 
coi'pus  callosum. 

The  body  is  composed  of  segments  placed  end  on  end,  and  there  is 
a  similar  distribution  of  the  nervous  system.  That  this  is  the  case 
with  the  greater  part  of  the  sympathetic  is  readily  recognized.  Each 
segment  of  the  body  is  represented  by  a  vertebra  and  its  appendages, 
and  most  of  the  vertebrae  have  a  corresponding  ganglion  for  each 
lateral  half,  although  fusion  of  two  or  more  ganglia  in  the  successive 
segments  of  the  cervical  region  and  in  those  of  the  coccyx  prevents  the 
correspondence  from  being  altogether  perfect. 

In  the  spinal  cord  the  analogous  ganglia  of  the  same  segment  and 
the  homologous  ganglia  of  successive  segments  have  become  so  com- 
pletely integrated  that  they  form  a  closed  tube  of  gray  matter,  which 
extends  from  the  conus  medullaris  up  through  the  whole  length  of  the 


ENCEPIIALO-SPINO-XEURAL    SYSTEM.  21 

cord,  the  floor  of  the  fourth  ventricle,  the  aqueduct  of  Sylvius,  and  the 
gray  matter  of  the  third  ventricle,  to  terminate  at  the  tuber  cinereum. 
One  consequence  of  the  fusion  of  homologous  ganglia  is  that  the  parts 
of  the  cord  which  correspond  to  the  diiferent  segments  of  the  body  have 
undergone  considerable  displacement.  The  cord  usually  ends  at  the 
lower  border  of  the  body  of  the  first  lumbar  vertebra- ;  but  the  nerves 
which  descend  to  pass  out  through  the  remaining  lumbar  intervertebral 
foramina  and  through  the  sacral  and  sacro-coccygeal  foramina,  show 
that  the  lower  part  of  the  cord  presides  over  the  functions  of  the  lower 
segments  of  the  body,  although  it  has  by  the  fusion  and  approximation 
of  the  homologous  centres  suffered  considerable  displacement. 

A  still  further  integration  has  taken  place  in  the  cephalic  centres,  and 
the  highest  ganglia — the  cerebrum  and  cerebellum — consist  of  large 
aggregations  of  gray  and  white  matter,  in  which  it  is  diflBcult  to  find 
any  trace  of  the  separate  ganglia  and  the  conducting  paths  of  which 
they  are  composed.  The  cephalic  ganglia,  spinal  cord,  and  peripheral 
nerves  form  one  functionally  indivisible  system  which  may  be  named 
the  encephalo-spino-neural  system. 


Encephalo-spino-neural  System, 

We  shall  now  make  a  few  general  remarks  on  (1)  the  arterial  supply 
of  this  system ;  (2)  its  topography ;  (3)  its  relations  to  the  skeleton ; 
(4)  the  topography  of  the  internal  parts  of  the  cerebrum,  as  being  the 
part  of  the  system  in  which  this  knowledge  is  most  generally  required 
for  practical  purposes;  and  (5)  the  internal  structure  of  the  system. 

1.    Tlie  Arterial  Supply, 
a.  The  Spinal  Arteries. 

(1)  The  spinal  branches  enter  the  intervertebral  foramina  along  with 
the  roots  of  the  spinal  nerves,  and  are  distributed  to  the  vertebrae, 
spinal  membranes,  and  spinal  cord.  These  arteries  are  derived  from 
the  lateral  sacral,  ilio-lumbar,  lumbar,  aortic  intercostal,  the  ascending 
cervical  branch  of  the  inferior  thyroid,  and  vertebral  arteries. 

(2)  The  anterior  spinal  artery  is  a  small  vessel  derived  from  the 
vertebral  artery  near  its  termination  in  tlie  basilar.  This  vessel  joins 
with  its  fellow  of  the  opposite  side  to  form  a  single  vessel  which  de- 
scends along  the  anterior  aspect  of  the  spinal  cord,  and  is  continued  to 
the  lower  end  of  the  cord  as  the  anterior  median  artery. 

(3)  The  posterior  spinal  artery  is  derived  froui  the  inferior  cerebellar 


22 


ANATOMICAL    INTKODUCTION 


artery ;  it  winds  round  the  medulla  oblongata  to  reach  the  posterior 
aspect  of  the  cord,  when  it  is  continued  onwards  to  the  cauda  equhia. 

(4)  The  nutritive  arteries  of  the  spinal  cord  are  sufficiently  indicated 
in  the  annexed  diagram  (Fig.  1). 


Fig.  1. 


la 
ea  a       \    m 


Diagram  of  the  Distribution  of  the  Bloodvessels,  and  Gbovping  or  Ganglion  Cells  in  the 
Spinal  Cord.    (Young.  ) 


Anterior  median  artery. 

(if,  Arteries  of  the  anterior  median  fissure. 

<ic,  Artery  of  the  anterior  commissure. 

1,  Anterior  branch. 
1',  Median  branch. 
1",  Posterior  branch. 

ca,  Central  artery. 

2,  Anterior  branch. 
2',  Median  branch. 
2",  Posterior  branch. 

pa,  Posterior  root  arteries. 

0  6'  6",  Arteries  of  posterior  horns. 
«Vt,  Internal  anterior  root  artery. 
CO,  External  anterior  root  artery. 

n  V.  Internal  and  external  branch. 


Antero-lateral  branch. 

4,  Anterior  branch. 

4',  Bledian  branch. 

4",  Posterior  branch. 
,  Median  lateral  artery. 

.5  5',  Anterior  and  posterior  branches 

Posterior  lateral  arteries. 

Internal  posterior  arteiy. 

Kxtcrnal  posterior  arteiy. 

Arteries  of  the  column  of  Goll. 

Artery  of  the  posterior  commissure. 

Vesicular  column  of  Clarke. 
Internal  group  of  cells. 

Anterior  group. 

Antero-lateral  group. 

Postero-lateral  group. 

Central  group. 

Median  area. 


ENCEPHALO-SPINO-NEUEAL    SYSTEM 


23 


b.  The  Arteries  of  the  Medulla  Oblongata,  Pons,  Crura  Cerebri,  and 

Cerebellum. 

(1)  The  vertebral  artery/  winds  backwards  round  tlie  articulating 
process  of  the  athis,  and,  after  piercing  the  dura  mater,  enters  the  skull 
tlirough  the  foramen  magnum,  and  terminates  at  the  lower  border  of 
the  pons  Varolii  bj  uniting  with  the  corresponding  vessel  of  the  oppo- 
site side  to  form  the  basilar  artery.    Besides  the  spinal  branches  already 


pia 


Section  of  the  Mebulla  Oblongata,  showing  the  Distribution  of  tiik  Vkssels. 
K,  Artery  of  the  Median  Kapbe. 

Ill,  Branches  to  the  formatio  reticularis. 
V,  Branch  to  the  olivary  body. 
1",  Branches  to  the  liypoglossal  nucleus. 

1'",  Branches  to  the  floor  of  the  fourth  ventricle,  and  to  the  internal  inferior  nuclei  of  the 
facial  [if). 


24  AXATOMICAL    INTRODUCTION. 

p.  Pyramidal  arteries, 
or,  Anterior  root  artery  (hypoglossal). 
2',  Branch  to  the  olivary  body. 

2",  Branches  to  the  formatio  reticnUris.     It  terminates  in  branches  to  the  hypoglossal  nucleus. 
Ir,  Lateral  root  artery  (vagus). 

.5,  Branch  to  the  restiform  body  and  the  inner  division  of  the  inferior  cerebellar  peduncle, 
o',  Branches  to  the  nucleus  of  the  vagus.    Also  gives  branches  to  the  ascending  root  of  the 
tifth  and  the  Jirrmidio  reticularis. 
ala.  The  anterior  lateral  artery  of  the  medulla  oblongata.     It  supplies  branches  to  the  formutio  reti- 
cularis, olivary  body,  anterior  nucleus  of  the  lateral  column  {olc\  and  terminates  in  branches 
to  the  hypoglossal  nucleus. 
mla.  The  middle  lateral  artery  of  the  medulla  oblongata.    It  supplies  branches  to  the  formatio  reli- 
mlaris,  the  posterior  nucleus  of  the  lateral  column  {pic),  and  terminates  in  branches  which  are 
distributed  to  the  external  accessory  nucleus  of  the  facial  (ef). 
phi,  The  posterior  lateral  arteries  of  the  medulla  oblongata.    They  supply  the  restiform  bodies. 
C,  Central  artery. 

:S  :i'  3",  Branches  to  tlie  liypoglo-ssal  and  external  accessory  facial  nuclei. 
mp,  Median  posterior  artery. 

4  4'  4",  Branches  to  tlie  external  accessory  facial  and  pneumogastric  nuclei. 
ep,  External  posterior  artery.     It  supplies  branches  to  the  internal  division  of  the  inferior  peduncle 

of  the  cerebellum  and  restiform  body. 
i.  Internal  group  of  cells  of  the  hypoglossal  nucleus. 
al,  Antero-lateral        "  " 

pi,  Postero-lateral       "  " 

a.  Anterior  " 

ale,  Anterior  nucleus  of  the  lateral  column. 
pic.  Posterior      "  " 

viii,  Inferior  portion  of  the  posterior  median  acoustic  nucleus. 
if,  Internal  accessory  facial  nuclei. 
ef,  External  accessory  facial  nucleus. 
/,  Fasciculus  rotundus. 
XII,  Ilypoglossal  nerve. 
X,  Pneumogastric  nerve. 
G,  Column  of  GoU. 

pr.  Posterior  root-zone.     The  direct  cerebellar  tract  forms  a  thin  band  lying  external  to  the  column  of 
GoU  and  posterior  root-zone. 
CM,  Clavate  nucleus. 
In,  Triangular  nucleus. 
0,  Olivary  body. 

po,  Parolivary  body. 
vp,  Nucleus  of  the  pyi'ainid. 
pn,  Nucleus  of  the  arciform  fibres. 
P,  Anterior  pyramid. 

al,  Ascending  root  of  the  trigeminus. 
ng.  The  substantia  gelatinosii. 

described,  tlie  vertebral  gives  rise  to  the  inferior  cerebellar  artery,  as 
well  as  to  meningeal  and  muscular  branches. 

(2)  The  basilar  artery  runs  forwards  in  the  groove  on  the  anterior 
surface  of  the  pons  Varolii,  and  divides  at  the  anterior  border  of  the 
pons  into  two  terminal  branches,  which  will  be  found  to  form  part  of 
the  circle  of  Willis.  The  branches  of  the  basilar  artery  are  the  trans- 
verse arteries  of  the  pons,  the  middle  and  superior  cerebellar  arteries, 
and  the  posterior  cerebral  artery.  These  branches  are  sufficiently  indi- 
cated in  the  annexed  diagram  (Fig.  2). 

(3)  The  nutritive  arteries  of  the  medulla  oblongata  and  pons  are 
shown  in  the  annexed  diagram  (Fig.  2). 


ENCEPH  A  LO-S  PINO- NEURAL    SYSTEM. 


25 


c.  The  Arteries  of  the  Cerebrum. 

(1)  The  posterior  cerebral  arteries  are  the  terminal  branches  of  the 
basihxr  trunk,  and  each  artery  winds  round  the  crus  cerebri  to  reach  the 
occipital  lobe. 

(a)  The  posterior  median  group  (Fig.  3,  2),  which  pierce  the  poste- 
rior perforated  space  and  supply  the  internal  surface  of  the  optic  thala- 
nius  and  the  walls  of  the  third  ventricle. 


Fig.  3. 


P-^ 


Diagram  of  the  Distribution  of  the  Ves^sels  at  the  base  of  the  Cerebrum.     (After  Charcot.) 
CA,  Anterior  cerebral  artery ;  S,  S,  Sylvian  arteries ;  V,  V,  Vertebral  arteries  ;  B,  Basilar ;  CP,  CP, 

Posterior  cerebral  arteries;   1,  2,  3,  3,  4,  4,  Groups  of  nutritive  arteries.     The  line limits  the 

ganglionic  vascular  area. 


(h)  The  poster 0-lateral  group  (Fig-  3,  4)  enter  the  brain  beliiiid  the 
border  of  the  crus  cerebri  and  pass  into  the  optic  thalamus  and  corpora 
quadrigemina. 

(e)  The  cortical  branches,  consisting  of  the  anterior  temporal,  the 
posterior  temporal,  and  the  occipital  arteries. 

(2)  The  anterior  cerebral  artery/  (Fig.  3,  CA),  derived  from  the 
internal  carotid  artery,  runs  forAvards  in  tlie  longitudinal  fissure,  and, 


26  ANATOMICAL    INTKODUCTION. 

turning  round  tlie  cm-pus  callosum,  is  distributed  to  the  anterior  part  of 
the  cerc'bruni.  The  arteries  of  the  two  sides  are  united  at  their  com- 
menceuient  by  a  short  transverse  branch,  the  anterior  communicating 

artery. 

(a)  The  anterior  median  group  (Fig.  3,  1)  supply  the  anterior  part 
of  the  head  of  the  caudate  nucleus. 

(6)  The  cortical  branches. 

(8)  The  middle  cerebral  or  Sylvian  artery  (Fig.  3,  S)  is  the  most 
important  branch,  and  the  direct  continuation  of  the  internal  carotid. 

(a)  The  antero-lateral  group  (Fig.  3,  3)  pierce  the  anterior  perforated 
space,  and  supjdy  the  corpus  striatum  and  anterior  part  of  the  optic 
thalamus. 

{h)  A  choroid  branch  Avhich  winds  round  the  crus  to  reach  the  choroid 

plexus. 

(c)  The  cortical  branches,  consisting  of  the  inferior  frontal,  the 
ascending  fi-ontal,  the  ascending  parietal,  the  parieto-sphenoidal  and 
sphenoidal  branches. 

(4)  The  posterior  communicating  artery  is  a  long  and  slender  vessel 
which  connects  the  internal  carotid  with  the  posterior  cerebral  arteries. 
These  two  arteries,  Avith  the  posterior  communicating  artery,  connect 
the  anterior  and  posterior  arterial  systems  of  the  brain,  and  complete 
the  anastomosis  round  the  circle  of  Willis  (Fig.  3). 

A  survey  of  the  arteries  of  the  brain  shows  that  they  may  be  divided 
into  (1)  the  vessels  which  are  distributed  to  the  cortex  of  the  brain — 
the  cortical  system  of  arteries;  and  (2)  those  which  pierce  the  base  of 
the  organ  to  supply  tlie  basal  ganglia — the  ganglionic  system. 

(1)    THE  CORTICAL  SYSTEM  OF  ARTERIES. 

The  arteries  of  the  cortical  or  nutritive  system  are  of  two  kinds  :  (a) 
the  long  or  medullary  arteries.,  and  (b)  the  short  or  cortical  arteries. 

(a)  The  long  or  medullary  arteries  pass  into  the  substance  of  the 
centrum  ovale  without  communicating  with  one  another,  except  by  fine 
capillaries,  and  consequently  each  constitutes  a  small,  independent 
vascular  territory.  These  vessels  extend  as  far  as  the  ganglionic  sys- 
tem, but  do  not  appear  to  anastomose  with  it. 

(b)  The  cortical  or  nutritive  arteries  arise  from  the  vascular  network 
of  the  pia  mater,  and  most  of  them  terminate  in  the  gray  matter ;  but 
a  few  of  them  send  capillaries  to  the  centrum  ovale. 

The  distribution  of  the  cortical  arteries  is  shown  in  the  annexed 
diagrams  (Figs.  4,  5,  and  6). 


EXCEPHALO-SPINO-NEURAL    SYSTEM.  27 

Fig.  4. 


View  of  the  Brain  fkom  below.     (After  Ecker  and  Duret.) 
Distribution  of  Vesseh. 

The  region  bounded  by  the  line  ( )  represents  the  territory  over  which  the  Internal  and  Inferior 

Frontal  Branches  of  the  Anterior  Cerebral  Artery  are  distributed. 

The  regions  bounded  by  the  line  ( )  represent  the  territories  over  whicli  the  branches  of 

the  Posterior  Cerebral  Artery  are  distributed 

I.  Is  the  region  of  tlie  Anterior  Temporal  Artery. 
II.         "  "  Posterior  Temporal  Arlerij. 

III.         "  "  Occipital  Artery . 

Fissures  and  Convolutions. 

Fl,  Gyrus  Eectus.  ti.  Sulcus  occipito-temporalis  inferior. 

J^2,  Middle  frontal  convolution.  t3,  Sulcus  temporo-sphenoidalis  inferior. 

FS,  Inferior  frontal  convolution.  12,  Sulcus  temporo-sphenoidalis  medialis. 

fi.  Sulcus  olfactorius.  x>o,  Parieto-occipital  fissure. 

/5,  Sulcus  orbitalis.  oc,  Calcarine  fissure. 

T2,  Second  or  middle  temporo-sphenoidal  convolution.  H,  Gyrus  hippocampi, 

rs,  Third  or  inferior  temporo-sphenoidal  convolution  U,  Gyrus  uncinatus. 

Ti,  Gyrus  occipito-temporalis  lateralis  (lobulus  fusi-  Ch,  Optic  chiasma. 

formis).  fc,  Corpora  albicantia. 

T5,  Gyrus  occipito-temporalis  medialis  (lobulus  lin-  KK,  Crura  cerebri, 

gualis  .  C,  Cori)us  callosum. 


28 


ANATOMICAL    INTRODUCTION 


(2)    THE  CENTRAL  OR  GAKGLIONIC  SYSTEM  OF  ARTERIES. 

The  ganglionic  system  form  six  main  groups,  which  are  named  the 
anterior'  an'd  posterior  median  (Fig.  3,  1  and  2) ;  the  right  and  left 
antero-lateral  (Fig.  8,  3,  3)  ;  and  the  right  and  left  posterolateral  (Fig. 
8,  4,  4).  An  imaijinary  line  passing  round  the  circle  of  Willis,  at  a 
distance  of  two  centimetres,  would  completely  surround  all  these  ves- 
sels, and  the  area  so  limited  may  be  called  the  ganglionic  vascular  area. 


Fig. 


Inner  Surface  of  Riuht  Hemisphere.     (After  Ecker  anJ  Dueet.) 

Distribution  of  Vessels. 
Tlie  regions  bounded  by  the  line  ( )  represent  the  territories  over  whicii  the  branches  of  the  Ante- 
rior Cerebral  Artery  are  distributed. 

I.  Is  the  territory  of  the  Interior  mid  Ankriur  Frontal  Artery. 
II.  "  "  Internal  and  Middle       "  " 

III.  "  "  Internal  and  Posterior    "  " 

The  regions  bounded  by  the  line  ( )  represent  the  territories  over  which  the  branches  of 

the  Posterior  Cerebral  Artery  are  distributed. 

II.  Is  the  territory  of  the  Posterior  Temporal  Artery. 
Ill-  "  "  Occipital  ilrtery . 

Fissttres  and  Convolutions. 
CC,  Corpus  callosum,  longitudinally  divided ;  Gf,  Gyrus  fornicatus ;  H,  Gyrus  hippocampi ;  h,  Sulcus 
hippocampi ;  U,  Uncinate  gyrus ;  cm,  Sulcus  calloso-marginalis  ;  Fj,  Median  aspect  of  the  first  frontal 
convolution  ;  c,  Terminal  portion  of  the  sulcus  centralis,  or  fissure  of  Rolando  ;  A,  Anterior ;  B,  Posterior 
central  convolution ;  Pj",  Precuneus ;  Oz,  Cuneus ;  Po,  Parieto-occipital  fissure  ;  o,  Sulcus  occipitalis 
transversus ;  oc,  Calcarine  fissure  ;  oc',  Superior,  oc".  Inferior  ramus  of  the  same  ;  D,  Gyrus  descendens ; 
T4,  Gyrus  occipito-temporalis  lateralis  (lobulus  fusiformis);  T5,  Gyrus  occipito-temporalis  medialis  (lobulus 
lingualis). 


EISrCEPHALO-SPINO-XEUEAL    SYSTEM, 


29 


All  these  vessels  are  terminal  arteries.     Some  of  these  branches  are  of 
sufficient  importance  to  have  been  specially  described  and  named. 


Fig.  6. 


Outer  Surface  of  the  Left  Hemisphere.     (After  K<kek  and  Duret.) 

Distribution  of  Fes.sefe. 

The  region  bounded  by  the  line  ( )  represents  the  territory  over  wliicli  branches  of  tlie  Anterior 

Cerebral  Artery  are  distributed. 

The  anterior  regions  bounded  by  the  line  ( )  represent  the  territories  over  which 

branches  of  the  Middle  Cerebral  Artery  are  distributed. 
I.  Is  the  region  of  the  External  and  Inferior  Frontal  Artery. 
II.  "  '■        Anterior  Parietal  Artery. 

III.  "  "        Posterior  Parietal  Artery . 

IV.  "  "        Parielo-sphenoidal  Artery 

Tlie  posterior  and  inferior  region  bounded  by  the  line  ( •- )  represents  the  territory 

over  which  branches  of  the  Posterior  Cerebral  Artery  are  distributed. 

Fissures  and  Convolutions. 
F,  Frontal  lobe.     P,  Parietal   lolx-.     0,   Occipital  lobe.     T,  Temporo-spheuoidal  lobe.    S,   Fissure  of 
Sylvius,  S'  Horizontal,  S"  Ascending  ramus  of  the  same,     c,  Sulcus  centralis  or  fissure  of  Eolando.    A 
Anterior  central  or  ascending  frontal  convolution.    B,  Posterior  central  or  ascending  parietal  convolution 
Fi  Superior,  r2  Middle,  and  F^  Inferior  frontal  convolutions,    /i  Superior  and  /»  Inferior  frontal  sulcus 
fs  Sulcus  prjecentvalis.      Pj  Superior  parietal  or  postero-parietal  lobule  ;  Po  Inferior  parietal  lobule,  viz. 
Po  Gyrus  supra-marginalis,   Pj'  Gyrus  angularis.     ip,  Sulcus  intra-parietalis      cm,  Termination  of  the 
calloso-marginal  fissure.     Oj  First,  Oj  Second,  O3  Third  occipital  convolutions,    po,  Parieto-occipital  fis 
sure,    o.  Sulcus  occipitalis  transversus ;  oj  Sulcus  occipitalis  longitudinalis  inferior.     Tj  First,  To  Second, 
T3  Third  temporo-sphenoidal  convolutions.     <i  First,  t«  Second  temporo-sphenoidal  fissures. 


50 


ANATOMICAL    INTRODUCTION, 


Branches  of  the  Middle  Cerebral  Artery. 

(a)  The  lenticular  branches  are  two  or  three  small  twigs  which  are 
distributed  to  the  two  inner  divisions  of  the  lenticular  nucleus  and  the 
adjoining  portion  of  the  caudate  nucleus  (Fig.  7,  5). 

(b)  The  lenticulo-striate  artery  ascends  between  the  external  capsule 
and  lenticular  nucleus,  and  supplies  the  outer  division  of  the  lenticular 
nucleus,  the  internal  capsule,  and  the  caudate  nucleus  (Fig.  7,  4). 

Fro.  7. 


Transverse  Section  of  the  Cerebral  Hemispheres,  about  1  cm.  behind  the  Optic  Commissure. 

(From  Buret.) 

Arteries  of  the  Corpus  Striatum. — Ch,  Chiasnia;  B,  Section  of  the  optic  tract ;  L,  Lenticular  nucleus; 
I,  Internal  capsule  ;  C,  Caudate  nucleus ;  E,  External  capsule  ;  T,  Claustrum ;  B,  Island  of  Reil  ;  F, 
V,  Section  of  the  lateral  ventricle  ;  P,  P,  Anterior  pillars  of  the  fornix ;  0,  Gray  substance  of  the 
third  ventricle. 

Vascular  Areas. — I,  Anterior  cerebral  artery;  II,  Middle  cerebral  artery;  III,  Posterior  cerebral 
artery. — 1,  Internal  carotid  artery  ;  2,  Sylvian  artery ;  3,  Anterior  cerebral  artery  ;  4,  4,  External 
arteries  of  the  corpus  striatum  (lenticulo-striate  artery) ;  5,  5,  Internal  arteries  of  the  corpus  striatum 
(lenticular  arteries).    The  opto-striate  artery  is  not  represented  in  the  figure. 

(c)  The  lenticulo-optic  artery  also  ascends  between  the  external  cap- 
sule and  the  lenticular  nucleus,  and  supplies  branches  to  the  posterior 
part  of  the  nucleus  and  of  the  internal  capsule,  and  terminates  in  the 
anterior  and  external  part  of  the  optic  thalamus. 

Branches  of  the  Anterior  Cerebral  Artery. 

The  anterior  median  group  supplies  the  anterior  part  of  the  caudate 
nucleus. 

Branches  of  the  Posterior  Cerebral  Artery. 

(a)  The  jJosterior  internal  artery  of  the  optic  thalamus  is  distributed 
to  the  internal  surface  of  that  oranglion. 


ENCEPHALO-SPIXO-NEURAL    SYSTEM.  31 

(b)  The  posterior  external  artery  of  the  optic  thalamus  is  distributed 
to  the  posterior  and  external  portion  of  that  ganglion,  and  also  sup- 
plies the  external  geniculate  bodies. 

2.   Topography  of  the  Encephalo-spino-neural  System. 

The  fissures  and  convolutions  of  the  cerebrum  are  suflSciently  indi- 
cated in  Figs.  4  to  6  -without  further  description.  The  cerebellum, 
pons,  and  medulla  oblongata  lie  at  the  base  of  the  skull  below  the 
tentorium,  the  spinal  cord  occupies  the  vertebral  canal  as  low  as  the 
inferior  border  of  the  body  of  the  first  lumbar  vertebra,  the  cranial 
peripheral  nerves  issue  through  various  foramina  at  the  base  of  the 
brain,  and  the  spinal  nerves  pass  through  the  intervertebral  foramina. 

3.    Relation   of  the  Different  Parts   of  the  Encephalo-spino-neural 
System  to  the  Skeleton, 
a.  Kelations  of  the  Spinal  Cord  and  Nerves  to  the  Vertebral  Canal. 
The  annexed  diagram  (Fig.  8)  shows  the  position  of  the  spinal  cord 
in  relation  to  the  vertebral  canal  in  which  it  lies.     The  tips  of  the 
cervical  spines  correspond  nearly  to  the  lower  borders  of  the  correspond- 
ing vertebrae.     Each  of  the  upper  three  dorsal  spines  corresponds  nearly 
to  the  upper  border  of  the  body  of  the  vertebra  below.     The  ninth, 
tenth,  and  eleventh  spines  slope  less,  and  their  tips  again  correspond  to 
the  upper  borders  of  the  next  vertebrae  below,  while  the  rest  of  the 
spines  are  opposite  the  bodies  of  their  own  vertebrae. 

b.  Kelations  of  the  Cerebral  Convolutions  to  the  Skull. 
The  convolutions  and  fissures  of  the  surface  of  the  brain  have  just 
been  described,  and  we  must  now  give  a  brief  account  (1)  of  the  topog- 
raphy of  the  surfiice  of  the  skull ;  and  (2)  of  the  relations  existing 
between  the  different  areas  of  the  skull  and  the  respective  convolutions 
and  fissures  of  the  brain. 

(1)  topography  of  the  external  surface  of  the  skull. 

The  topography  of  the  external  surface  of  the  skull  has  been  studied 
by  Broca,  Fere,  Turner,  and  others,  with  the  view  of  connecting  defi- 
nite points  and  areas  on  the  surface  with  the  respective  convolutions 
and  fissures  of  the  brain.  We  shall  adopt  the  divisions  and  descrip- 
tions of  Turner  in  this  place : 

Definite  Landmarks  on  the  Surface  of  the  Skull. — The  following 
structures  and  markings  are  easily  recognized  on  the  skull.  The  ex- 
ternal occipital  protuberance  (Fig.  9,  o),  the  parietal  (P)  and  frontal  (F) 


32 


ANATOMICAL    INTRODUCTION, 


eminences,  and  tlie  external  angular  process  of  the  frontal  bone  (A), 
the  coronal  {c)  and  lambdoidal  (Z),  squamous  (s),  squamoso-sphenoid 


Fig.  8. 


Diagram  showing  the  Relation  of  the  Spines  of  the 

Vertebr.t:  to  the  Origin  of  the  Nerves. 

(After  GowEits.) 

The  first  three  cervical  spiues  are  upiiosite  the  origins  of 
the  od,  4th,  and  5th  cervical  nerves.  The  6th  and  7th  pairs 
arise  opposite  the  intervals  between  the  4th  and  5th  and  the 
5th  and  6th  cervical  spines  respectively  The  6th  cervical 
siiine  corresponds  to  the  origin  of  the  8th  cervical  nerve, 
and  the  7th  cervical  spine  to  the  first  dorsal  nerve.  The 
first  four  dorsal  spines  vary.  The  1st  spine  corresponds  to 
the  interval  between  the  2d  and  3d  pairs,  or  to  the  origin  of 
tlie  .3d  pair.  The  2d  spine  is  between  the  3d  and  4th  pairs, 
or  opposite  the  4th  pair  The  3d  spine  is  opposite  the  5th, 
or  the  interval  between  the  5th  and  Gth  pairs.  The  4th 
spine  is  opposite  the  lower  part  of  the  origin  of  the  6th 
pair,  or  even  below  it  The  5th  spine  always  corresponds 
to  the  origin  of  the  7th  pair;  the  6th  spine  to  the  8th  pair ; 
the  7th  to  the  9th  pair ;  the  8th  to  the  ui)per  part  of  the 
loth  pair ;  the  9th  to  the  11th  pair  ;  and  the  10th  to  the 
12th  pair.  The  1st  lumbar  arise  opposite  the  11th  dorsal 
spine  ;  the  second  lumbar  opposite  the  interval  between  the 
11th  and  12th  spines  ;  the  3d  and  4th  ojiposite  the  12th 
spine  ;  the  5th  lumbar  and  the  1st  sacral  opposite  the  inter- 
val between  the  12th  dorsal  and  1st  lumbar  spines,  while 
the  remaining  sacral  nerves  arise  nearly  opposite  the  1st 
lumbar  spine. 

The  cervical  enlai-gement  of  the  cord  corresponds  nearly 
to  the  bodies  and  spines  of  the  cervical  vertebrae,  while  the 
lumbar  enlargement  corresponds  to  the  bodies  of  the  11th 
and  12th  dorsal  and  1st  lumbar  vertebras,  and  to  the  lower 
three  dorsal  and  1st  lumbar  spines. 


ENCEPHALO-SPINO-NEURAL    SYSTEM.  33 

(ss),  and  parieto-splienoid  sutures  (ps),  and  the  curved  line  of  the  tem- 
poral ridge  (t). 

Primary  Areas  of  the  Skull. — The  coronal  suture  (c)  forms  the 
posterior  boundary  of  the  frontal  area.  A  vertical  line  (Fig.  9,  2) 
drawn  from  the  squamous  suture  (s)  upwards  through  the  parietal  emi- 
nence (P)  to  the  sagittal  suture  lies  almost  parallel  to  the  coronal  suture, 


Fig.  ;i. 


Latkral  View  ui'  the  Hujian  Skull.     (Feuriee.  ) 

A,  The  external  angular  process  of  the  frontal  bone.  F,  The  frontal  eminence.  P,  The  iiarictal  emi- 
nence. 0,  The  occipital  protuberance,  c,  The  coronal  suture.  I,  The  lambdoidal  suture  s,  The  squa- 
mous suture,  t,  The  temporal  ridge,  /s,  The  fronto-sphenoid  suture,  ps,  The  parieto-sphenoid  suture. 
ss,  The  squanioso-sphenoid  suture,  pm,  Tlie  parieto-mastoid  suture  1,  Frontal  line.  2,  Parietal  line. 
SF,  MF,  IF,  The  supero-,  mid-,  and  infero-frontal  subdivisions  of  the  frontal  area.  SAP,  Tlie  supero- 
antero-parietal  area.  lAP,  The  infero-antero-jjarietal  area.  SPP,  The  siipero  postero-parietal  area. 
IPP,  The  infero-postero-parietal  area.  0,  Tlie  occipital  area.  Sq,  The  sijuamoso-tem])oral  area.  AS, 
The  ali-sphenoid  area. 


and  subdivides  the  parietal  region  into  an  antero-parietal  (Fig.  9, 
SAP-f  lAP)  and  a  postero-parietal  area  (Fig.  9,  SPP  +  IPP). 
The  occipital  region  lies  between  the  lambdoidal  suture  (l)  and  the 
occipital  protuberance  (o),  with  the  superior  cui'ved  line  extending  from 
it  (Fig.  9,  o). 

Secondary  Areas  of  the  Skull. — These  four  primary  divisions  of  the 
skull   may  be  subdivided  into   secondary  areas.     The  temporal  ridge 


34  ANATOMICAL    INTEODUCTION. 

(Fig.  9,  t).  Starting  from  the  external  frontal  process,  curves  backwards 
across  the  frontal  (A),  antero-iiarietal,  and  post-parietal  areas  to  the 
internal  angle  of  the  occipital  bone,  and  subdivides  each  of  these  re- 
gions into  an  upper  and  a  lower  area.  The  upper  frontal  area,  which 
includes  all  the  frontal  regions  above  the  temporal  ridge,  is  again  di- 
vided by  a  line  drawn  vertically  upwards  and  backwards  from  above  the 
orbit  through  the  frontal  eminence  to  the  coronal  suture  (Fig.  9,  c). 
This  line  divides  the  upper  frontal  area  into  a  supero-frontal  (SF)  and 
a  mid-frontal  area  (MF). 

Two  other  areas  remain  to  be  described.  These  are  concealed  by  the 
temporal  muscle,  and  are  limited  superiorly  by  the  squamoso-parietal, 
sphenoido-parietal,  and  fronto-sphenoidal  sutures.  The  lines  of  the 
sutures  naturally  divide  this  area  into  a  squamoso-temporal  (Sq)  and 
ali-sphenoidal  area  (AS). 

The  following,  then,  are  the  secondary  areas  of  the  skull :  Superior 
Frontal  (SF),  3Iiddle  Frontal  (MF),  Inferior  Frontal  (IF),  Upper 
Antero-parietal  (SAP),  Lozver  Antero-parietal  (lAP),  Ujjper  Postero- 
parietal  (SPP),  Lower  Fostero-jyarietal  (IPP),  Occipital  (0),  Squa- 
moso-tem^joral  (Sq),  and  Ali-sphenoidal  (AS). 

(2)    RELATIONS    OF    THE    DIFFERENT    AREAS    OF    THE    SKULL    TO    THE    RESPECTIVE 
CONVOLUTIONS    AND    FISSURES. 

The  fissure  of  Sylvius  (Fig.  10,  SS)  commences  behind  the  posterior 
border  of  the  lesser  wing  of  the  sphenoid,  and  courses  upwards  and 
backwards  below  the  greater  wing  of  the  sphenoid,  where  this  articu- 
lates with  the  anterior  inferior  angle  of  the  parietal  bone,  and  then 
appears  in  the  lower  part  of  the  inferior  antero-parietal  region.  The 
fissure  of  Rolando  (Fig.  10,  R)  lies  in  the  antero-parietal  region,  both 
in  its  superior  and  inferior  divisions,  its  upper  extremity  being  as  much 
as  two  inches  and  its  lower  an  inch  and  a  half  behind  the  respective 
ends  of  the  coronal  suture.  The  coronal  suture  does  not,  therefore, 
correspond  to  the  boundar}-  between  the  frontal  and  parietal  lobes  of 
the  brain. 

The  parieto-occipital  fissure  (Fig.  10,  PO)  is  situated  on  an  average 
about  0.7  to  0.8  inch  in  front  of  the  apex  of  the  lambdoidal  suture. 

Contents  of  the  Respective  Areas. 

The  frontal  area  is  occupied  by  the  frontal  lobe,  but  does  not  cover 
the  whole  of  it,  the  posterior  extremities  of  the  three  frontal  convolu- 
tions lying  behind  the  coronal  suture.  The  frontal  area,  therefore, 
corresponds  to  the  part  of  the  frontal  lobe  supplied  by  the  anterior 
cerebral  artery,  and  which  is  not  excitable  to  stimulation.     The  supe- 


EXCEPIIALO-SPINO- NEURAL    SYSTEM, 


35 


rior,  middle,  and  inferior  frontal  areas  of  the  skull  correspond  respec- 
tively to  the  superior,  middle,  and  inferior  frontal  convolutions,  with 
the  exception  of  their  posterior  extremities. 

The  uppe7'  antero-parietMl  area  (Fig.  10,  SAP)  contains  the  upper 
two-thirds  of  the  ascending  frontal  (AP)  and  ascending  parietal  (S) 


Fig   10. 


DiAGKAM  showing;  the  Relations  of  the  Convolutions  to  the  Skull.  (Turner.) 
K,  The  fissure  of  Rolando,  which  separates  the  frontal  from  the  parietal  lobe.  PO,  The  parieto-occipi- 
tal  fissure  between  the  parietal  and  occipital  lobes.  SS,  The  fissure  of  Sylvius,  which  separates  the  tem- 
poro-spheuoidal  from  the  frontal  and  parietal  lobes.  SF,  MF,  IF,  The  supero-,  mid-,  and  infero-froutal 
subdivisions  of  the  frontal  area  of  the  skull  :  the  lettei-s  are  placed  on  the  superior,  middle,  and  inferior 
frontal  convolutions  SAP,  The  superoantero  parietal  area  of  the  skull :  S  is  placed  on  the  ascending 
parietal  convolution,  AP  on  the  ascending  frontal  convolution.  lAP,  The  infero-antero-parietal  area  of 
the  skull  :  I  is  placed  on  the  ascending  parietal,  AP  on  the  ascending  frontal  convolution.  SPP,  The 
supero-postero-parietal  area  of  the  skull  :  the  letters  are  placed  on  the  angular  convolution.  IP?,  The 
infero-postero-parietal  area  of  the  skull :  the  letters  are  placed  on  the  mid-teraporo-sphenoidal  convolu- 
tion. Xj  The  convolution  of  the  parietal  eminence,  or  supra-marginal  gyrus.  0,  The  occipital  area  of 
the  skull :  the  letter  is  placed  on  the  mid- occipital  convolution.  Sq,  The  squamoso-temporal  region  of 
the  skull :  the  letters  are  placed  on  the  niidtemporo-sphenoidal  convolution.  AS,  The  ali-sphenoid 
region  of  the  skull  :   the  letteis  are  placed  on  the  tip  of  the  supero-temporo-s])henoidal  convolution. 


convolution,  and  the  posterior  extremities  of  the  superior  (1.2  in.)  and 
middle  frontal  (1.3  in.)  convolutions.  At  the  upper  posterior  angle  of 
this  area  part  of  the  postero-parietal  lobule  is  visible,  and  below  this 
part  of  the  supra-marginal  lobule  may  appear. 

The  lower  antero-parietal  area  (Fig.  10,  lAP)  contains  the  lower 


36  ANATOMICAL    INTRODUCTION. 

third  (if  tlie  ascending  parietal  (1  in.)  and  ascending  frontal  (AP)  con- 
volutions, and  the  posteriin-  extremities  (1  in.)  of  the  inferior  frontal 
convolution.  A  small  portion  of  the  supra-marginal  gyrus  is  visible  at 
the  upper  posterior  angle  of  this  area,  and  below  it  a  small  portion  of 
the  sujierior  temporo-splienoidal  convolution. 

The  upper  poster o-parletal  area  (Fig.  10,  SPP)  contains  the  greater 
part  of  the  postero-parietal  lobule.     Below  it  lies  the  upper  portion  of 
the  angular  gyrus  (SPP),  and  part  of  the  supra-marginal  gyrus  (X) 
Posteriorly  the  annectant  gyri  blend  with  the  occipital  lobe. 

The  loiver  postero-parietal  area  (Fig.  10,  IPP)  contains  part  of  the 
supra-marginal  gyrus,  and  behind  it  part  of  the  angular  gyrus,  and 
below  this  the  posterior  or  upper  ends  of  the  temporo-sphenoidal  con- 
volutions. 

The  occipital  area  (Fig.  10,  0)  indicates  the  situation  of  the  occipital 
lobe,  but  is  not  coextensive  with  it,  inasmuch  as  a  portion  extends 
anteriorly  beyond  the  lambdoidal  suture  into  the  postero-parietal  area. 

The  squamoso-temporal  area  (Fig.  10,  Sq)  contains  the  greater  por- 
tion of  tlie  temporo-sphenoidal  convolutions,  but  the  superior  temporo- 
sjjhenoidal  convolution  ascends  into  the  lower  parietal  areas. 

The  ali-sphenoidal  area  (Fig.  10,  AS)  contains  the  lower  or  anterior 
extremity  of  the  temporo-sphenoidal  lobe. 

The  central  lobe,  or  Island  of  Reil,  does  not  come  to  the  surface,  but 
lies  deep  in  the  fissure  of  Sylvius,  and  is  concealed  by  the  convolutions 
which  form  the  margin  of  that  fissure  anteriorly.  It  lies  opposite  the 
ui)per  part  of  the  great  wing  of  the  sphenoid  and  its  line  of  articulation 
with  the  anterior  inferior  angle  of  the  parietal  and  the  squamous  part 
of  the  temporal. 

The  convolutions  situated  on  the  internal  aspect  of  the  hemisphere 
are  altogether  out  of  relation  to  the  surface  of  the  skull. 

The  deep-seated  position  and  direction  of  the  hippocampal  region  are 
superficially  indicated  by  the  convolutions  of  the  temporo-sphenoidal 
lobes,  contained  chiefly  in  the  inferior  postero-parietal,  squamoso-tem- 
poral, and  ali-sphenoidal  areas. 

4.   TopjOLirapliy  of  tlie  Internal  Parts  of  the  Cerebrum. 

The  anatomy  of  the  cerebrum  is  most  conveniently  studied  by  suc- 
cessive horizontal  and  vertical  sections. 

Centrum  Ovale. 
A  horizontal  section  made  half  an  inch  above  the  corpus  callosum 
displays  the  white  matter  of  each  hemisphere  surrounded  on  all  sides 


E  X  C  E  P  H  A  L  O  -  S  P  I N  O  -  X  E  Tj  R  A  L    S  Y  S  T  E  :N  F , 


37 


by  the  giay  matter  of  the  convolutions.  The  white  central  mass  in 
each  hemisphere  was  named  by  Vicq.  d'Azyr  the  centrum  ovale  minus. 
A  section  made  at  the  level  of  the  corpus  callosum  shows  that  the  white 
substance  of  that  part  is  continuous  with  the  central  white  substance  of 


Fig.  11. 


Hdrizom  AT,  Section  of  the  Brain  of  a  Child  nine  months  of  aue,  the  right  side  being  at  a 

SOMEWHAT   lower   LE\T:L  THAN   THE   LEFT  HALF.     (After  FLECHSIG.) 

F,-  Frontal,  TS,  Temporo-sphenoidal,  and  0,  Occipital  lobes;  Op,  Operculum;  In,  Island  of  Kei! ;  CU, 
Clanstrum  ;  /",  Third  frontal  convolution  ;  Th,  Optic  thalamus  ;  NC,  Caudate  nucleus  ;  iVC,  Tall  of  cau- 
date nucleus ;  LN,  Lenticular  nucleus ;  I,  II,  III,  First,  second,  and  third  divisions  of  the  lenticular 
nucleus ;  EK,  External  capsule  ;  IK,  Posterior  division,  IE',  Anterior  division,  and  K,  Knee  of  the  inter- 
nal capsule  ;  ah,  ph.  Anterior  and  posterior  horns  respectively  of  the  lateral  ventricles  ;  gcc,  Knee  of  the 
corpus  callosum  ;  sp,  Splenium ;  mc,  Middle  commissure ;  f.  Fornix ;  si,  Septum  lucidum ;  a,  Cornu 
Animonis. 


each  hemisphere.  The  large,  white  medullary  mass  thus  displayed  is 
named  the  centrum  ovale  majus.  The  corpus  callosum  connects  the 
convolutions  of  one  cerebral  hemisphere  with  corresponding  points  in 


38  ANATOMICAL    INTEODUCTION  . 

the  convolutions  of  the  other.  It  consists  of  bundles  of  nerve  fibres, 
almost  the  whole  of  which  pass  transversely  between  the  two  hemispheres, 
although  a  few  fibres  run  longitudinally  on  its  surface,  named  the  strice 
longitudinales  or  nerves  of  Laneisi. 

A  horizontal  section  nearer  to  the  base  of  the  brain  reveals  the  basal 
ganglia  and  the  internal  capsule,  as  represented  in  Fig.  11. 

A  svstematic  nomenclature  of  the  various  parts  of  the  centrum  ovale 
has  been  devised  by  Pitres.  His  system  consists  in  making  vertical 
sections  of  the  brain  at  definite  points,  and  naming  the  various  parts  of 
the  medullarv  sidjstance  exposed  in  each  section.  A  vertical  section  of 
the  hemisphere  at  right  angles  to  its  longitudinal  axis  in  the  pra-frontal 
region  gives  the prcefrontal  sectmi(F\g.  V2).    The  next  section  is  made 

Fig.  12. 


Pe  KFEONTAL  SECTION.      (After  PiTRES.) 

1,  2,  3,  First,  second,  and  third  frontal  convolutions.    4,  Orbital  convolutions.    5,  «'onAi)Uitioii3  on  the 
internal  aspect  of  the  frontal  lobe.    6,  Prsefrontal  fasciculi  of  the  centrum  ovale. 

two  centimetres  in  front  of  the  fissure  of  Rolando  and  passes  througli 
the  bases  of  the  three  frontal  convolutions,  and  is  named  the  pedunculo- 
frontal  section  (Fig.  13).  The  medullarv  substance  in  this  section  is 
subdivided  into  a  superior,  middle,  and  an  inferior  pedunculofrontal 
fasciculus,  corresponding  with  the  respective  frontal  convolutions. 
The  next  section  is  made  through  the  ascending  frontal  convolution, 
parallel  with  the  fissure  of  Rolando,  and  is  named  the  frontal  section. 
It  also  passes  through  a  small  portion  of  the  sphenoidal  lobe.  The 
medullary  substance  of  this  section  is  also  subdivided  into  sujjerior, 
middle,  and  inferior  frontal  fasciculi  (Fig.  14).  The  fourth  section 
is  carried  through  the  ascending  parietal  convolution,  and  is  named  the 
parietal  section.     It  is  subdivided  into  superior,  middle,  and  inferior 


ENCEl'IIALO-SPINO-XEURAL    SYSTEM.  39 

parietal  fasciculi  (Fig.  15).     The  next  is  the  j^cdunculo-panetal  sec- 
tion, made  by  dividing  the  hemisphere  three  centimetres  behind  the 


Fig.  1?,. 


lO 

y 

■""■'* 

n 

V 

m 

12 

/3 

ff- 

-:■      ^W 

9 

\^ 

:^;^ 

■A    8 

1^3 


Peduncui-o-fuumai,  Skction.     (Aftei-  Pitees.) 
1,  2,  3,  Fii-st,  second,  and  third  frontal  convolutions.    4,  Anterior  extremity  of  the  insular  lobe.    .5, 
Posterior  extremity  of  the  orbital  convolutions.     6,  Superior  pedunculo-frontal  fasciculus.    7,  Middle 
pednnculo-frontal  fasciculus.     8,  Inferior  pedunculo-frontal  fasciculus.    9,  Orbital  fasciculus.     10,  Corpus 
callosum.     11,  Caudate  nucleus.     12,  Internal  capsule.     13,  Lenticular  nucleus. 


Fig.  14. 


Feontal  Section      (After  Pitres.) 
1,  Ascending  frontal  convolution.    2,  Insular  lobule.    3,  Sphenoidal  lobe,     i,  5,  6,  Superior,  middle, 
and  inferior  frontal  fasciculus.     7,  Sphenoidal  fasciculus.    8,  Corpus  callosum.    9,  Caudate  nucleus.    10, 
Optic  thalamus.     11,  Internal  capsule.     12,  Lenticular  nucleus.     13,  External  capsule.    14,  Claustrum. 


40  ANATOMICAL    INTRODUCTION, 

Fig.  15. 


Tarietat,  Section.    (After  Pitres.) 
1.  Ascending  iiarietal  convolution.     2,  Insular  lobe.     3,  Sphenoidal  lobe.     4,  Superior  parietal  fas- 
ciculus.   5,  Middle  parietal  fasciculus.     0,  Inferior  parietal  fasciculus.     7,  Sphenoidiil  fasciculus.     >S,  9, 
10,  11,  12,  13,  14,  as  in  the  preceding  figure. 


Fig.  10. 


PEnUNCULO-PARIETAL  SECTION.      (After  PlTRES.) 

1,  Superi(  r  parietal  lobule.  2,  Inferior  parietal  lobule.  3,  Sphenoidal  lobe.  4,  Superior  pedunculo- 
parietal  fasciculus.  5,  Inferior  pedunculo-parietal  fasciculus  0,  Sphenoidal  fasciculus.  7,  Coi  pus  cal- 
losum.     8  and  10,  Caudate  nucleus,     ii,  Optic  thalanui:^. 


EXCEPH  ALO  -  SPIXO  -  X  K  U  R  AL    SYSTEM  , 


41 


fissure  of  Rolando,  and  cutting  the  superior  and  inferior  parietal  lobules. 
It  is  subdivided  into  superior  and  inferior  pedunculo-parietal  and 
sphenoidal  fasciculi  (Fig.  16). 

The  last  is  the  occipital  section  (Fig.  17),  in  which  no  separate  fas- 
ciculi are  distinguished. 

Fig.  17. 


l>(CIPirAI,  Sfctiiin.      {  MtCI  rilRES  ) 
1,  Occiiiital  convolutions,     i,  Occipital  fasciculi  of  the  centrum  ovale. 

5.   The  Internal  Structure  of  the  Eneephalo-spino-neural  System. 
The  internal  structure  of  the  encei)halo-spino-neural    system  must 
now  be  briefly  described,  and  for  this  purpose  we  shall  divide  the  sys- 
tem into  (1)  the  spino-neural,  and  (2)  the  encephalo-spinal  systems. 

(1)  The  Spino-neur-vl  System. 
A  spinal  segment  consists  of  a  disk  of  nervous  matter  to  each  lateral 
half  of  which  a  nerve  is  attached  by  an  anterior  and  posterior  root,  the 


The  Anteriok  Surface  of  the  Spinal  SEfiMENT,  the  Anterior  Eoot  of  the  Eight  Side  being 
Divided.    (After  Allen  Thomson,  from  Quain.) 

1,  The  anterior  median  fissure ;  2,  Posterior  median  fissure ;  3,  Anterior  lateral  depression,  over  which 
the  anterior  nerve  roots  are  seen  to  spread ;  4,  Posterior  lateral  groove  into  which  the  posterior  roots  are 
seen  to  sink ;  5,  Anterior  roots  passing  the  ganglion ;  5',  The  anterior  root  divided ;  6,  The  posterior 
roots,  the  fibres  of  which  pass  into  the  ganglion,  6' ;  7,  The  united  or  compound  nerve ;  7',  The  posterior 
primary  branch  seems  to  be  derived  in  part  from  the  anterior  and  in  part  from  the  posterior  root. 

latter  being  furnished  with  a  ganglion  (Fig.  18).     The  gray  substance 
which  represents  the  gangliated  structure  occupies  the  central  parts  of 


4-2 


ANATOMICAL    INTllODUCTION 


the  cord  in  the  well-known  shape  of  the  letter  H.  The  median  part  of 
the  orav  substance  contains  the  central  canal  and  the  central  gray 
nucle'us  of  Kolliker,  the  anterior  gray  and  white  commissure  lying  in 


Fig.  ]0 


Section  from  the  Midpi.e  of  the  Cervical  Eni-aroemknt  ..f  the  Sri>Ai.  Cokd  at  the  Third 

Month  of  Embryonic  Life. 

C,  Central  canal.     The  other  lettei-s  indicate  the  same  as  tlie  conespomling  lettei-s  in  Fig  1. 


Fig.  20 


i,  internal ; 
ganglion  cells 
group. 


Spinal  Cord  of  a  Five-months  Human  Embryo,  from  the  Middle  ok  the  Cervk.al 

and  Lumbar  Enlargements  Respectively.    (YouNfi  ) 
a,  anterior  ;   a\  antero-lateral ;  p/,  postero-lateral,  c,  central,  and  m,   median  groups  of 
:  1,  ganglion  cell  of  the  centre  of  the  antero-lateral  group;  2,  ganglion  cell  of  the  median 


E  X  C  E  P  H  A  L  O  -  S  P  I N  O  -  X  E  U  R  A  L    S  Y  S  T  E  :^r 
Fig.  •_'•_'.  Fig.  23. 


Sf.itioks  of  Spinal  Curd  of  a  Xine-moxths  Human-  Embryo,  from  tHf,  Middle  of  the  Lumbar 
AND  Ceevk'al  Enlargements  Respectively.    (Young.) 
A,  anterior,  and  P,  posterior  horns.     Tlie  small  letters  indicate  the  same  as  in  Figs.  20  and  21.    The 
normal  size  of  the  .•action  from  which  the  di-awing  was  made  is  shown  above  each  figure. 


Fig.  24. 


Fig.  25. 


Sections  of  the  Adult  Spinal  Cord  from  the  Middle  of  the  Lumbar  and  Ckrvical  Enlargements 

Kespectively.    (Young  ) 

The  letters  indicate  the  same  as  those  in  Figs.  20  and  21. 


u 


ANATOMICAL    INTRODUCTION. 


front,  and  the  posterior  commissure  behind  it.  The  hiteral  parts  or 
coluimis  consist  of  an  anterior,  middle,  and  posterior  part,  the  first  of 
them  representing  the  anterior,  and  the  Last  the  posterior  gray  horn, 
and  the  middle  chiefly  the  vesicular  column  of  Clarke. 

The  anterior  horns  contain  large  ganglion  cells,  each  of  which  is 
furnished  with  numerous  branched  processes  by  means  of  which  it 
forms  definite  connections  with  other  cells  and  fibres.  One  of  these 
processes  is  unbranched,  and  it  becomes  continuous  with  the  axis-cylin- 
der of  an  efierent  fibre  which  passes  out  through  the  anterior  root  and 
nerve  to  the  periphery.  The  ganglion  cells  of  the  posterior  horn  are 
much  smaller  and  less  branched  than  those  of  the  anterior  horns,  and 
this  horn  receives  afferent  fibres  from  the  periphery  of  the  body. 


Fio.  20. 


Fio.  2^ 


Sections  of  the  Ahui.t  Uimax  Simnal  Cord,  from  the  Upper  Cervicai,  axd  1J"R.s.vi.  Keoioxs 

Respectively.    (Young.) 
A,  anterior,  and  P,  posterior  liorns;  aa,  anterior  roots;  cc,  central  canal;  ml,  the  meilio-lateral  area. 
The  other  letters  indicate  the  same  as  the  corresponding  ones  in  Figs.  20  and  21      The  size  of  the  sections 
from  which  the  drawing  was  talcen  is  indicated  above  each.     In  Fig.  27,  vc  represent;*  tlio  vesicular 
column  of  Clarice. 

In  the  development  of  the  gray  matter  of  the  cord,  the  groui)S  of 
ganglion  cells  appear  first  in  the  anterior  and  lateral  margins  of  the 
anterior  horn  (Fig.  19),  where  they  form  several  distinct  groups,  which 
are  as  far  as  possible  removed  from  the  central  canal.  The  gray  matter 
surrounding  the  central  canal  represents  the  growing  or  embryonic  por- 


ENCEPIIAT.O-SPINO-NEUEAL    SYSTEM.  45 

tion  of  tlie  gray  luuttor,  and  every  new  ganglion  cell  which  develops 
becomes  su])eradded  at  the  margins  of  the  first  forward  groups.  The 
groups  of  ganglion  cells  are  i)retty  constant  for  the  same  portions  of  the 
c<»rd,  but  the  arrangement  varies  considerably  when  sections  at  different 
elevations  are  compared.  These  groups  are  represented  in  the  annexed 
diagrams  (Figs.  20-27),  and  are  named  the  |)Ostero-lateral  {pt),  the 
antero-lateral  {at),  the  anterior  (a),  the  internal  (/),  and  the  central  (c) 
groups  respectively.  Another  area — the  median  (m) — contains  in  tlie 
adult  human  cord  a  considerable  number  of  caudate  cells  of  small  size, 
although  they  are  not  aggregated  into  a  distinct  group.  The  cells 
of  the  median  area,  and  of  the  margins  of  the  groups,  representing  the 
latest  evolved  structures,  will  be  the  counterpart  of  the  latest  evolved 
functions.  The  last  evolved  purely  spinal  function  (not  taking  into 
account  those  regulated  from  the  medulla  oblongata)  are  the  complicated 
movements  of  the  hand,  and  it  may  therefore  be  expected  that  the 
median  area  and  the  marginal  cells  will  be  more  fully  developed  in  the 
cervical  enlargement  than  in  any  other  part  of  the  cord,  in  the  adult 
cord  than  in  the  embryo,  and  in  the  hunuin  cord  than  in  the  cord  of 
animals.  This  expectation  is  fully  borne  out  by  these  facts.  A  very 
distinct  grouj)ing  of  ganglionic  cells  lies  in  the  posterior  gray  horn  near 
the  posterior  commissure,  named  the  vesicular  column  of  Clarke  (Fig.  1, 
ve).  So  far  we  have  only  spoken  of  one  segment  of  tlie  cord,  but  the 
gray  matter  of  the  different  segments  has  become  integrated  to  such  an 
extent  that  it  forms,  not  a  series  of  ganglia  like  the  sym])athetic  sj^stem, 
but  a  continuous  tube.  The  central  gray  tube  opens  at  the  calamus 
sci'iptorius  into  the  fourth  ventricle,  while  higher  up  it  is  represented 
by  the  aqueduct  of  Sylvius,  and  then  opens  into  the  third  ventricle. 
In  the  medulla  the  groups  of  ganglion  cells  ha\'e  undergone  an  exten- 
sive rearrangement.  The  main  grouj)  of  the  anterior  horns  is  repre- 
sented by  the  nuclei  of  origin  of  the  hyi»oglossal  nerve  (Fig.  2,  ^',  a, 
ah  pi),  but  a  portion  of  the  antero-lateral  and  ])ostero-lateral  groups 
have  become  detached  from  the  rest  of  their  groups,  and  are  aggregated 
in  the  formatio  reticularis  in  two  tolerably  distinct  groups,  the  anterior 
and  posterior  nuclei  of  the  lateral  column  of  the  medulla  (Fig.  2, 
ale,  pic).  The  median  area  and  the  nuirginal  cells  are  represented  by 
a  much  larger  ao-o-regation  of  cells  than  anything  to  be  found  in  the  cord, 
and  constitute  groups  which  may  be  named  the  internal  accessory 
(Fig.  2,  if)  and  the  external  accessory  nuclei  (Fig.  1,  ef)  of  the  facial 
nerve.  These  groups  of  cells  are  probably  the  structural  counterparts 
of  mimetic  facial  and  articulatory  movements. 

The  vesicular  column  of  Clarke  is  only  represented  in  the  dorsal 
region  of  the  spinal  cord.     It  contains  bipolar  ganglion  cells,  and  cells 


46 


ANATOMICAL    INTRODUCTION. 


of  similar  character  are  to  be  found  in  the  nuclei  of  the  vagus  (Fig. 
2,  nv)  and  glosso-pliaryngeal  nerves,  and  it  is  therefore  probable  that 
the  nuclei  of  these  nerves  are,  to  some  extent  at  least,  the  representa- 
tives of  the  vesicular  column  of  Clarke  in  the  medulla. 


Fig.  28. 


Section  of  the  Meduli,.\  Obuin(:.\ta  on  a  levkl  with  the  supbrfici.\t.  orkmn  of  the  Acoustic  Nerve. 

(Modified  from  Flechsig.) 
E  vm,  Boot  uf  the  acoustic  nerve. 

VIII,  Posterior  median  acoustic  nucleus 

Tin",  Posterior  lateral  acoustic  nucleus. 

H,  Nucleus  of  the  hypoglossal  nerve. 
ip,  Internal  division  of  the  inferior  peduncle  of  the  cerebellum. 
ep,  External  division  of  the  inferior  peduncle  of  the  cerebellum. 
frs,  Forniatio  reticularis. 
a,  Arciform  iibres. 

The  posterior  gray  horn  is  represented  in  the  medulla  by  the  sub- 
stantia gelatinosa  (Fig.  2,  sg).  In  addition  to  the  sensory  nuclei  of 
common  sensation  represented  by  the  substantia  gelatinosa,  the  medulla 
oblongata  contains  special  sensory  nuclei.     It  is  probable  that  part  of 


ENGEPHALO-SriNO- NEURAL    SYSTEM. 


47 


the  nuclei  of  the  gh)8so-i)haryiige!il  nerve,  and  probably  also  of  the  fifth 
nerve,  reiiresent  the  special  nerves  of  taste;  four  nuclei,  namely,  the 
posterior  median  (Fig.  28,  Viii),  the  posterior  lateral  the  anterior  median, 
and  the  anterior  lateral  acoustic  nuclei,  represent  the  auditory  nerve; 
Avhile  the  corpora  quadrigemina  and  the  internal  geniculate  body  repre- 
sent the  nuclei  of  origin  of  the  optic  nerve.  The  spinal  ganglia,  situ- 
ated in  the  })Osterior  roots  of  each  pair  of  nerves,  belong  to  the  spinal 
system.  The  casserian  ganglion  is  the  representative  of  these  ganglia 
in  the  cranial  end  of  the  spinal  system.  The  middle  sensory  nucleus  of 
the  trigeminus  is  also  in  structure  very  similar  to  the  ganglia  of  the 
posterior  roots,  and  it  also  is  probably  the  homologue  of  the  spinal 
ganglia.  The  external  geniculate  hody  likewise  contains  cells  which  are 
very  like  those  of  the  ganglia  of  the  posterior  roots,  and  it  must  possibly 
be  regarded  as  a  ganglion  for  the  optic  nerve  homologous  with  the 
spinal  ganglia. 


«/* 


Transversje  Section  of  the  Cervical  Part  or  the  Spinal  Cord  of  a  Human  Embryo  of  six  weeks. 

(From  KoLLiKER.) 

c,  Central  cuiial ;  e,  e',  Its  eiiithelial  lining  ;  g,  Gray  substance  ;  ar,  Anterior  roots  ;  pr,  Posterior  roots  ; 

a,  Anterior  root-zones  ;  p,  Posterior  root-zones. 


The  white  substance  of  a  sjiinal  segment  is  divided  anatomically  by 
the  anterior  and  posterior  median  fissure,  and  the  nerve  roots  into  an 
anterior,  lateral,  and  posterior  column  for  each  lateral  half.  A  small 
portion  only  of  this  white  substance  really  belongs  to  the  spinal  system, 
the  remainder  representing  conducting  paths  between  the  portions  of 
the  cord  below,  or  posterior  to  the  segment  examined,  and  the  encephalic 
ganglia.  This  purely  spinal  portion  of  the  white  substance  consists  of 
the  portions  named  the  anterior  and  jyosterior  root-zones.  As  might 
be  expected,  these  areas  are  the  first  portions  of  the  white  substance  to 


48  ANATOMICAL    INTRODUCTION.  | 

appear  in  the  development  of  the  cord,  an<l  they  are  consequently  least 
distinguislied  at  an  early  period  of  embryonic  life.  During  the  first 
Aveeks'^of  embryonic  life  the  cord  consists  entirely  of  gray  matter  in 
the  form  of  a  tube,  Avhich,  by  the  appearance  of  lateral  slits,  is  imper- 
fectly divided  into  anterior  and  posterior  portions.  Toward  the  end  of 
the  first  month  a  zone  of  white  substance  appears  on  the  surface  of  the 
anterior  and  posterior  portions  of  the  gray  tube,  and  there  constitute 
respectively  the  anterior  and  posterior  root-zones  (Fig.  29,  a,p).  Tliese 
zones  are  supposed  to  consist  of  short  looped  fibres,  the  posterior  one 
coordinating  the  functions  of  the  gray  substance  on  the  sensory  or 
ino-oing  side,  and  the  anterior  on  the  motor  or  outgoing  side. 

The  most  important  fact  with  regard  to  the  distribution  of  these 
zones  is  that,  at  any  level  of  the  cord,  they  correspond  in  size  to  that 
of  the  gray  substance,  these  zones  being,  like  the  gray  substance,  of 
comparatively  large  size  in  the  lumbar  and  cervical  enlargements. 

The  jjosterior  root-zone  (Fig.  2,  pr),  on  being  followed  upwards 
into  the  medulla  oblongata,  will  be  found  to  terminate  in  the  gray 
nucleus  of  the  cuneate  fasciculus,  the  triangular  nucleus  ;  but  the  tracts 
of  Avhite  substance  known  as  the  ascending  root  of  the  fifth  nerve  (Fig. 
2,  at),  the  fasciculus  rotundus  (Fig.  2,  /),  and  the  descending  root 
of  the  fifth  nerve  are  the  homologues,  in  the  cranial  portion  of  the 
spinal  system,  of  the  posterior  root-zones  of  the  cord.  i 

The  anterior  root-zone,  on  being  followed  upwards  into  the  medulhi 
oblongata,  is  seen  to  be  separated  up  into  bundles  by  the  arcuate  fibres 
of  the  medulla,  and  the  interlacement  of  the  two  systems  of  fibres 
forms  what  is  knoAvn  as  the  formatio  reticularis  (Fig.  28,  frs).  The 
anterior  root-zone  consists  of  two  portions :  an  internal  (Fig.  37,  ar), 
which  lies  to  the  inner,  and  an  external  (Fig.  37,  ar'j,  which  lies  to 
the  outer  side  of  the  anterior  roots. 

The  internal  portion  of  the  anterior  root-zone  is  puslied  aside  in  the 
lower  part  of  the  medulla  by  the  decussating  fibres  of  the  pyramidal 
tracts ;  but  above  the  level  of  the  decussation  it  is  thrust  backwards 
behind  the  anterior  pyramid  of  the  medulla,  and  is  situated  between 
the  median  raphe  and  the  fibres  of  the  hypoglossal  nerve  (Fig.  2,  ar) 
In  the  spinal  cord  the  internal  portion  of  the  anterior  root-zone  main- 
tains a  close  relationship  with  the  internal  group  of  ganglion  cells,  and 
this  portion  of  the  root-zone  is  most  probably  represented  in  the 
medulla  oblongata,  pons,  and  crura  cerebri  by  the  bundle  of  fibres 
named  the  posterior  longitudinal  fasciculus  (Fig.  2,  ar).  This  fas- 
ciculus is  said  by  Wernicke  to  be  connected  with  the  first  division  of 
the  lenticular  nucleus  by  the  fibres  which  form  the  anterior  portion  of 
the  collar  of  the  crus  cerebri. 


EXCEPIIALO-SPIXO-XEURAL    SYSTEM.  49 

The  external  jjortion  of  the  anterior  root-zone  of  the  spinal  cord  is 
continued  upwards  into  the  formatio  reticularis  of  tlie  medulla  oblon- 
gata (Fig.  28,  ar').  This  portion  lies  behind  the  olivary  body,  and 
comes  to  the  surface  of  the  medulla  in  its  lateral  column  ;  while  it  is 
bounded  internally  by  the  root-fibres  of  the  anterior  motor  nerves,  ex- 
ternally by  the  root-fibres  of  the  nerves  of  the  lateral  mixed  svstem, 
and  posteriorly  by  gray  matter.  The  interlacing  fibres  of  the  pons 
(Fig.  47,  Tr)  pass  in  front  of  this  portion  {ar'),  and  in  the  crus  it 
comes  again  further  forwards,  so  that  it  is  only  separated  from  the  crusta 
by  the  locus  niger  (Fig.  40,  ar'). 

The  Fillet. — The  portion  of  the  anterior  root-zone  which  lies  next 
to  the  inner  and  posterior  surfaces  of  the  olivary  body  in  the  medulla, 
an<l  to  the  interlacing  fibres  of  the  pons,  is  named  the  fillet.  It  is 
divided  into  an  internal  and  an  external  portion  corresponding  to  the 
internal  and  external  divisions  of  the  anterior  root-zone.  The  internal 
portion  lies  to  the  inner  side  of  the  olivary  body,  a  part  of  it  even 
coming  in  front  of  that  body,  and  between  it  and  the  anterior  pyramid 
(Fig.  28,  ar).  Above  the  line  of  the  olivary  body  this  last  portion  is 
pushed  backwards  so  as  to  join  the  external  portion,  and  both  divisions 
now  lie  behind  the  transverse  fibres  of  the  pons.  The  fibres  of  the 
internal  division  of  the  fillet  seem  to  pass  upwards  to  become  connected 
with  the  optic  thalamus,  while  those  of  the  external  division  (Fig.  36, 
x'  and  x)  subdivide  into  an  outer  and  inner  bundle,  the  former  of  Avhich 
terminates  in  the  posterior,  and  the  latter  in  the  anterior  tubercle  of 
the  corpora  quadrigemina. 

(2)  The  Encephalo-spinal  System. 

The  encephalo-spinal  system  consists  of  a,  the  gray  substance  of  the 
cerebellum  ;  6,  the  gray  substance  of  the  cerebrum  ;  and  c,  the  con- 
ducting paths  which  connect  these  gray  masses  with  one  another  and 
with  the  central  gray  tube. 


a.    THE    GRAY    SUBSTANCE    OF    THE    CEFvEBRUM. 

(1)  The  Cortex  Cerebri. — By  far  the  greater  portion  of  the  gray 
substance  of  the  cerebrum  is  disposed  up  the  surface  of  the  cerebral 
hemispheres.  The  cortical  substance  consists  of  cells  and  fibres  em- 
bedded in  a  matrix  similar  to  the  neuroglia  of  the  spinal  cord. 

The  cells  are  of  various  forms,  the  most  usual  forms  being  spherical, 
stellate,   pyramidal,  and  fusiform.     The  fibres  radiate  into  the  gray 

4 


50 


ANATOMICAL    INTRODUCTION, 


Fig.  30 


Transparent  Sfxtion  of  a  Furrow  of 
THE  Third  Cerebral  Convolution  of 
Man.  Magnified  100  decimetres.  (After 
Meynert.) 

1,  Layer  of  the  scattered  small  cortical 
corpuscles ;  2,  Layer  of  close-set,  small 
pyramidal  corpuscles ;  3,  Layer  of  large 
pyramidal  cortical  corpuscles  i  formation 
of  the  coruu  Ammonis) ;  4,  Layer  of  small, 
close-set,  irregular-shaped  cortical  corpus- 
cles fgranule-like  formation)  ;  5,  Layer  of 
fusiform  cortical  corpuscles  (claustral 
formation) ;  m,  the  medullary  lamina. 


cortex  from  tlie  wliite  centre  of  each  con- 
volution, their  course  being  vertical  to 
the  free  surfoce  of  the  convolution.  They 
are  arranged  in  bundles  as  they  pass 
through  the  gray  substance,  and  this 
o:ives  to  the  nerve-cells  a  columnar  ar- 
rano-ement.  The  radiating  fibres  are 
wanting  in  the  sulci  between  the  convo- 
lutions, but  the  internal  layer  of  the 
gray  substance  of  the  cortex  generally 
contains  fibres  which  ])ursue  an  arciform 
course  and  connect  adjacent  convolutions. 
Fibres  pass  in  all  directions  through  the 
gray  substance  connecting  its  several 
layers,  and  forming  a  dense  network, 
like  that  described  by  Gerlach  in  the 
spinal  cord. 

Layers  of  the  Cortex. — The  cortex  of 
the  cerebrum  is  divided  into  several 
layers,  each  of  which  possesses  a  definite 
histoloo-ical  character.  The  most  com- 
monly  distributed  form  of  structure  is 
what  Meynert  has  called  the  "five 
laminated  type."  The  external  layer  con- 
sists of  neuroglia  and  a  layer  of  delicate 
nerve-tubes,-  along  with  a  few  scattered 
small  nerve-cells  which  are  destitute  of 
processes.  The  next  layer  is  composed 
of  small  angular  or  pyramidal  nerve-cells 
with  branching  processes.  The  third 
layer  contains  large  and  small  pyramidal 
cells  Avith  branching  processes,  arranged 
with  their  pointed  extremities  towards 
the  surface  of  the  convolutions,  and 
separated  into  groups  by  bundles  of  the 
radiating  fibres.  In  the  innermost  por- 
tion of  this  layer  the  pyramidal  cells  are 
larger  than  in  the  remaining  portions, 
and  it  has  therefore  been  described  as  a 
separate  layer  by  Dr.  Lockhart  Clarke. 
In  the  cortex  of  the  occipital  lobe  the 


encephalo-spino-np:ural  system.  51 

deeper  cells  of  the  third  layer  are  pyramidal  in  form,  with  their  bases 
turned  inwards  towards  the  medullary  substance,  but  their  basal  pro- 
cesses are  directed  laterally  so  as  to  connect  adjacent  cells,  and  none 
of  them  appear  to  be  directed  inwards  to  connect  the  cells  with  the 
fibres  of  the  medullary  substance.  In  the  anterior  portion  of  the 
frontal  convolutions  the  disposition  of  these  cells  is  somewhat  similar, 
but  a  distinct  basal  process  has  occasionally  been  observed,  which  is 
directed  towards  the  medullary  substance  of  the  convolution,  and  which 
afterwards  becomes  continuous  with  one  of  the  fibres  of  the  centrum 
ovale. 

In  the  central   convolutions  of  the  brain,   Betz   and  Mierzejewski 
have  discovered  cells  which  are  tAvo  or  three  times  the  size  of  the  pvra- 

FiG.  31. 


Pyramidal  Giant-cell. 
»,  Nucleus  ;  «,  «,  «,  Branched  processes  ;  c,  UnbraDched  basal  process. 

midal  cells  of  the  other  regions  of  the  cortex,  and  they  have  conse- 
quently named  them  giant  cells.  In  addition  to  the  branched  proto- 
plasmic processes  (Fig.  31,  a,  a)  which  connect  neighboring  cells  with 
one  another,  these  cells  possess  a  distinct  axis-cylinder  process  (Fig.  31,  c). 
The  latter  is  always  unbranched,  and  after  becoming  surrounded  by  a 
medullary   sheath  it  forms  the  axis-cylinder  of  a  nerve-fibre   of  the 


52 


ANATOMICAL    INTRODUCTION, 


centrum   ovale.     Giant  cells  have   been   observed  in   the  paracentral 
lobule  and  in  a  portion  of  the  postero-parietal,  as  well  as  in  the  ascend- 


ScHEiviA  (IF  THE  CEREDRo-sriNAL  SYSTEM.  (From  Landols's  Phijuiologie.) 
C,  C,  Cortex  of  the  Brain ;  0  s,  Corpus  Striatum ;  X  I,  Lenticular  Nucleus  ;  T  o,  Optic  Tlialanms ; 
V,  Corpora  Quadrigemina ;  P,  Crura  Cerebri;  H,  Tegmentum;  j),  Crusta;  1  1,  Eadiate  Filires  of  the 
Corpus  Striatum  ;  2  2,  those  of  the  Lenticular  Nucleus  ;  3  3,  those  of  the  Optic  Tlialamus  ;  4  4,  those  of  the 
Corpora  Quadrigemina  and  Tegmentum;  5  5,  the  Pyramidal  Tract;  fi  G,  Fibres  connecting  the  Corpora 
Quadrigemina  and  Tegmentum  ;  m,  their  further  co\irse  ;  8  8,  Fibres  connecting  the  C'orpus  Striatum  and 
Lenticular  Nucleus  with  the  Crusta;  M,  their  further  course  ;  S  S,  course  of  the  Sensory  Fibres,  11,  Trans- 
verse Section  of  the  Spinal  Cord  ;  v  W,  Anterior,  and  h  W,  Posterior  Hoots  of  the  Nerves,  a  a,  associat- 
ing Fibres  ;  c  c,  Commissural  Fibres.  II,  Transverse  Section  through  the  Crura  Cerebri  of  Man  on  a 
level  with  the  posterior  pair  of  the  Corpora  Quadrigemina  (after  Meynert)  ;  p,  Crusta  ;  S,  Locus  Niger; 
V,  the  posterior  pair  of  the  Corpora  Quadrigemina  with  the  A(iueduct  of  Sylvius.  Similar  sections  from 
the  Crura  of — III,  Dog  ;  IV,  Monkey  ;  V,  Guinea-pig. 


ENCEPHALO-SriXO-NEURAL    SYSTEM.  53 

ing  frontal  and  parietal  convolutions,  and  posterior  extremities  of  the 
three  frontal  gyri.  These  cells  are  disposed  in  groups,  and  correspond 
in  position  to  the  motor  centres  of  physiologists.  The  giant  cells  vary 
greatly  in  size,  the  largest  being  found,  as  we  have  already  seen,  in 
the  paracentral  lobule,  Avhich  may  be  regarded  as  the  upper  extremity 
of  the  ascending  frontal  and  parietal  convolutions.  Large  pyramidal 
cells  are  also  met  with  in  the  upper  part  of  the  ascending  frontal  con- 
volutions, and  Dr.  Bevan  Lewis  has  found  that  they  diminish  in  size 
from  the  upper  extremity  until  at  the  lower  extremity  they  are  but  half 
the  size.  The  pyramidal  cells  of  the  posterior  extremities  of  the  frontal 
convolutions  are  on  the  whole  smaller  than  those  of  the  ascendino- 
frontal,  and  the  cells  also  diminish  from  above  downwards,  those  in 
Brocas  convolution  being  the  smallest. 

The  fourth  layer  consists  of  closely  set  angular  corpuscles  with  fine 
processes,  placed  irregularly  and  not  distinctly  separated  into  groups. 

The  fifth  layer  consists  of  medium  sized,  fusiform,  and  bipolar  cells. 
The  long  diameters  of  these  cells  run  parallel  to  the  layers  of  the 
cortex,  and  are  associated  with  the  system  of  fibres  which  connects  dif- 
ferent convolutions  of  the  same  hemisphere  with  one  another. 

(2)  The  Basal  'or  the  Intermediate  Cerebral  Cranglia. — Several 
masses  of  gray  matter  are  situated  at  the  base  of  the  cerebral  hemi- 
spheres, there  occupying  an  intermediate  position  between  the  cortex 
cerebri  and  the  central  gray  tube.  These  ganglia  are  the  caudate 
nucleus  (Fig.  32,  C  s),  the  lenticular  nucleus  (Fig.  32,  N  T),  the  optic 
thalamus  (Fig.  32,  T  o),  the  locus  niger,  the  corpora  quadrigemina 
(Fig.  32,  V),  and  the  internal  geniculate  body.  The  corpus  striatum 
is  sometimes  used  to  designate  the  caudate  nucleus  alone,  wdiile  at  other 
times  it  is  used  as  a  generic  term  for  both  the  caudate  and  lenticular 
nuclei.  Although  we  have  included  the  corpora  quadrigemina  amongst 
the  intermediate  cerebral  ganglia,  we  have  already  seen  some  reason  to 
regard  them  as  being  the  homologues  of  the  posterior  gray  horns  of  the 
spinal  cord. 

b.    THE   GRAY    SUBSTANCE    OF    THE    CEREBELLUM. 

(1)  The  Cortex  CerehellL — The  greater  portion  of  the  gray  sub- 
stance of  the  cerebellum  is  also  disposed  on  the  surface,  Avhere  it  forms 
numerous  lartiince  or  folia,  which  are  separated  by  fissures  or  sulci  of 
different  depths. 

(2)  The  Intermediate  Cerebellar  G-anglia. — Occupying  the  central 
part  of  the  lateral  lobe  of  the  cerebellum  is  a  folded  mass  of  gray 
matter  named  the  corpus  dentatum ;  and  Stilling  has  described  two 
small  masses  of  gray  matter  which  are  situated  in  the  anterior  end  of 
the    inferior   vermiform    process,   and  which    he    named    roof  nuclei. 


54  ANATOMICAL    INTRODUCTION. 

These,  then,  are  the  only  masses  of  gray  matter  which  are  to  be  found 
in  the' cerebellum  itself;  but  the  inferior,  middle,  and  superior  pedun- 
cles are  connected  with  other  aggregations  of  gray  substance  in  the 
medulla  oblongata,  pons,  and  crura  cerebri,  and  these  must  also  be 
regarded  as  belonging  most  probably  to  the  cerebellar  system.  The 
chief  of  these  masses  of  gray  matter  are  the  olivary  bodies,  which  are 
connected  with  the  inferior  peduncle  of  the  cerebellum  of  the  opposite 
side  (the  late  researches  of  Flechsig  appear  to  cast  some  doubt  upon 
this  statement) ;  the  red  nucleus  of  the  tegmentum,  which  is  connected 
with  the  superior  peduncle  of  the  cerebellum  of  the  opposite  side ;  and 
the  <n-ay  matter  interposed  between  the  transverse  fibres  of  the  pons, 
and  which  is  connected  with  the  middle  peduncle  of  the  cerebellum  also 
of  the  opposite  side.  The  parolivary  body,  the  superior  olivary  body, 
and  the  nucleus  of  tie  pyramid  are  other  small  aggregations  of  gray 
matter  having  a  structure  somewhat  similar  to  that  of  the  corpus  den- 
tatum  of  the  cerebellum,  the  olivary  body,  and  the  red  nucleus  of  the 
tegmentum,  but  their  connections  are  not  yet  made  out.  In  addition 
to  these  are,  in  the  lateral  and  posterior  part  of  the  medulla  oblongata, 
the  triangular  nucleus,  in  which  the  posterior  root-zones,  and  the 
clavate  nucleus,  in  which  the  column  of  Goll,  to  be  immediately  de- 
scribed, terminate. 

C.    THE    ENCEPHALO-SPINAL    CONDUCTING    PATHS. 

The  purely  spinal  portion  of  the  spinal  cord  consists,  as  we  have 
seen,  of  the  central  gray  tube,  with  its  commissures  and  attached 
nerves,  and  the  anterior  and  posterior  root-zones.  Now  these  portions 
of  the  cord  form  more  or  less  direct  connections  with  the  encephalic 
ganglia.  The  central  gray  tube  is  directly  connected  with  the  optic 
thalamus  by  means  of  the  gray  matter  which  lines  the  third  ventricle. 
The  anterior  root-zone  is  connected  with  the  lenticular  nucleus  by 
means  of  the  posterior  longitudinal  fasciculus,  with  the  optic  thalamus 
by  means  of  the  internal  portion  of  the  fillet,  and  with  the  corpora 
quadrigemina  through  the  external  portion  of  the  fillet.  The  greater 
portion  of  the  posterior  root-zone  terminates  in  the  triangular  nucleus 
(Fig.  33,  tn)  of  the  medulla  oblongata,  and  this  nucleus  is  connected 
by  means  of  arcuate  fibres  (Fig.  33,  11)  with  the  olivary  body  (Fig. 
33,  0)  of  the  same  side,  which  in  its  turn  is  connected  with  the  inferior 
peduncle  of  the  cerebellum  of  the  opposite  side. 

We  must  now  pass  on  to  describe  the  special  conducting  paths  which 
connect  the  central  gray  tube  with  the  higher  ganglia,  and  a  knowledge 
of  these  is  best  obtained  by  a  study  of  the  development  of  the  cord. 

At  the  end  of  the  first  month  of  embryonic  life  the  spinal  cord  con- 


E  X  C  E  1'  H  A  T,  O  -  S  1'  I  X  u  -  X  E  L'  R  A  T,    SYS  T  E  M 
Fkj.  33. 


55 


Schema  of  the  Cekebellospinal  System. 
C,  (',  Cortex  of  the  Cerebellum.  D,  D,  Corpora  Deutata.  0,  0,  Olivary  Bodies.  E,  Ked  Xucleus  of 
Tegmentum  P,  Gray  matter  interposed  between  transverse  Fihi-es  of  the  Pons.  CR,  Crura  Cerebri.  C, 
Ci-usta.  .S,  Substantia  Nigra.  T,  Tegmentum.  A,  A(iucduct  of  Sylvius.  1,  Fibres  which  connect  the 
cortex  of  the  Cerebrum  and  that  of  the  Cerebellum  on  the  opposite  side.  2,  2,  Fibres  connecting  the 
Cortex  of  Cerebellum  and  Red  Xucleus  of  the  opposite  side.  3,  3,  Fibres  connecting  the  Corpus  Dentatum 
of  the  Cerebellum  with  the  Red  Xucleus  of  the  opposite  side.  4,  4,  Fibres  connecting  the  Cortex  of  the 
Cerebellum  with  the  Corpus  Dentatum  5,  Fibres  connecting  the  Cortex  of  the  Cerebellum  with  Gray 
substance  interposed  between  the  transverse  Fibres  of  the  Pons  on  the  opposite  side.  G,  Fibres  connect- 
ing the  .Corpus  Dentatum  with  the  Olivary  body  of  the  opposite  side.  7,  Fibres  connecting  the  Cortex  of 
the  Cerebellum  with  the  Olivary  body  of  the  opposite  side.  8,  8,  Fibres  connecting  the  Red  Xucleus. 
9,  !l,  those  connecting  the  interposed  Gray  substance  of  the  Pons,  and  9",  those  connecting  the  Olivarj' 
l(ody  respectively  with  the  anterior  Gray  Horn  of  the  Spinal  Cord.  M,  The  Anterior  Column  of  the  cord 
through  which  the  fibres  piiss.  g,  Column  of  GoU  terminating  in  en  the  Clavate  Xucleus  10,  Arcuate 
Fil)res  connecting  the  Clavate  Xucleus  with  the  Olivary  body  of  the  same  side,  p  r,  The  Posterior  Root- 
zone  terminating  in  tu,  the  Triangular  Xucleus  11,  Arcuate  Fibres  connecting  Triangular  Xucleus  and 
Olivary  body  of  same  side,  dc,  dc,  Direct  Cerebellar  Fibres  ascending  in  the  lateral  column  of  the  cord 
and  connecting  the  vesicular  column  of  Clarke  with  the  Cortex  of  the  Cerebellum. 


5(3  ANATOMICAL    IXTRODUCTION . 

sists  of  a  tube  of  gray  matter  with  a  layer  of  white  substance  on  its 
anterior  and  posterior  aspects,  a  portion  of  the  lateral  surface  of  the 
tube  being  uncovered.  At  the  end  of  the  sixth  week  a  thm  layer  of 
white  substance  appears  on  each  lateral  surface,  and,  as  the  fibres  of 
this  layer  are  found  to  pass  to  the  cerebellum,  they  have  been  named 
the  direct  cerebellar  fibres  of  the  lateral  column.  At  the  end  of  the 
eidith  week  of  embryonic  life  still  further  changes  are  observed  to 
ocair  in  the  cord.  Two  bundles  of  longitudinal  fibres,  one  for  each 
side,  are  intercalated  between  the  direct  cerebellar  fibres  and  the  pos- 
terior gray  horns.  These  bundles,  on  being  traced  upwards,  are  found 
to  pass  forwards  at  the  lower  end  of  the  medulla,  and  after  decussating 
with  one  another,  they  push  aside  the  anterior  columns  and  form  the 
inner  and  larger  portion  of  the  anterior  pyramids  of  the  medulla,  and 
consequently  these  fibres  are  called  the  lateral  pyramidal  tracts  (Fig. 
34^  P^  P'y    Contemporaneously  with  the  formation  of  the  lateral  pyra- 

FiG.  34. 


Cord  op  Human  Emukyo  at  Fivi;  Months. 


'tjTi 


ah,  ah',  Anterior  Horns  of  gray  substance  ;  j)/i,  j)7(',  Posterior  Horns  of  gray  substance;  ar,  ar',  .\n- 
terior  Root-zones;  pr,  pr',  Posterior  Koot-zones ;  P,  P,  Pyramidal  Fibres  of  lateral  columns;  T,  t'ol- 
umns  of  Tiirck  ;  G,  Columns  of  Goll ;  dc,  dc',  Direct  cerebellar  fibres  ;  c.  Anterior  Commissure. 


niidal  tracts  an  analogous  formation  appears  in  the  anterior  columns, 
one  of  these  being  formed  on  each  side  of  the  anterior  median  fissure. 
These  tracts  have  been  called  the  columns  of  Tiirck,  or  of  Lockhart 
Clarke,  or  the  anterior  pyramidal  tracts  (Fig.  34,  T).  At  the  same 
time  that  these  changes  are  occurring  in  the  lateral  and  anterior  col- 
umns, two  bundles  of  longitudinal  fibres  make  their  appearance  in  the 
posterior  columns,   one  being  situated   on   eacli   side  of  the  posterior 


EXCEPHALO-SPIXO- NEURAL    SYSTEM. 


57 


ft        P 


en  G 


f  M  vm    ^P 

T   ar 


Fig.  35. 

(After  FLECiisin  ) 

G,  The  column  of  Goll. 

J))-,  the  posterior  root-zone. 

J),  the  posterior  root. 

r,  the  posterior  gray  horn. 

A,  the  anterior  gray  horn. 

dc,  the  direct  cerebellar  tract. 

j)t,  the  lateral  pyramidal  tract 

T,  the  anterior  pyramidal  tract 

fr,  the  formatio  reticxilaris. 

or',  the   external   portion   of   the 

anterior  root-zone. 
ar,  the  internal  portion  of  the  an- 
terior root-zone. 
(it,  the  ascending  root  of  the  fifth 

nerve. 
Sg,  the  substantia  gelatinosa. 
tn,  the  triangular  nucleus 
en,  the  clavate  nucleus. 
P  and  P',  the  anterior  pyramids  of 

the  medulla  oblongata. 
//,  the  jillet. 
po,  the  parolivary  body, 
o,  the  olivary  body, 
e/i,  the  external   division   of  the 
inferior    peduncle    of    the 
cerebellum. 
ip,  the  internal  division  ot  the  in- 
ferior peduncle  of  the  cere- 
bellum. 
ale  and  j.)?c,  anterior  and  pot^terior 
nuclei  of  the  lateral  column. 
/".  fasciculus  rotundus. 
VIII,  posterior  median  nucleus  of 

the  auditory  nerve 
XII,  the  micleus  of  the  hypoglos- 
sal nerve. 


G   P^ 


58  ANATOMICAL  INTKODUCTION . 

median  fissure.  These  fibres  are  called  the  coluiims  of  Goll,  or  tlie 
postero-medimi  columns  (Fig.  34,  Gf).  The  anterior  white  commis- 
sure also  appears  about  the  eighth  week.  A  most  important  fact  to 
notice  in  connection  with  the  development  of  the  white  substance  is 
that  the  fibres  when  first  developed  are  destitute  of  a  medullary  sheath, 
and  only  become  mcdullated  at  a  late  period  of  development.  When 
the  cord  of  a  human  embryo  is  examined  at  the  end  of  the  fifth  month, 
it  will  be  found  that  the  pyramidal  fibres  of  the  lateral  columns,  the 
fibi-es  of  the  columns  of  Tiirck,  and  the  columns  of  Goll  are  non-medul- 
lated,  while  the  fibres  of  the  anterior  and  posterior  root-zones,  and 
those  of  the  direct  cerebellar  tracts  are  medullated.  When  a  transverse 
secti(m  of  the  cord  is  examined  in  glycerin  after  hardening  in  chromic 
acid,  the  bundles  composed  of  the  non-medullated  fibres  Avill  be  found 
to  transmit  the  light  more  readily  than  those  composed  of  the  medul- 
lated fibres,  and  consequently  a  section  of  the  cord  of  a  hunuin  embryo 
at  the  fifth  month  presents  in  the  cervical  region  the  appearances  repre- 
sented in  Fig.  34.  The  embryological  tracts  are  represented  diagram- 
raatically  in  Fig.  35.  The  portion  of  the  lateral  column  which  adjoins 
the  gray  matter  is  named,  from  its  i-eticulated  appearance,  the  formatio 
reticularis  (Fig.  35,  fr).  This  part  of  the  cord  is  composed  chiefly  of 
longitudinal  fibres  of  small  diametei',  and  the  reticulated  appearance  is 
given  to  it  partly  by  the  passage  through  it  of  a  considerable  number 
of  horizontal  fibres  from  the  vesicular  column  of  Clarke  to  reach  the 
direct  cerebellar  tract,  and  from  the  ganglion  cells  of  the  anterior  gray 
horns  to  reach  the  lateral  ])yramidal  tract,  and  ])artly  by  the  hmgitudi- 
iial  fibres  being  separated  by  comparati\ely  wide  septa  of  neuroglia. 
The  formatio  reticularis  appears  indeed  oidy  to  be  a  better  developed 
part  of  the  anterior  root-zone,  and  it  is  not  known  to  perform  any 
special  functions.  The  spinal  part  of  the  encephalo-spinal  conduct- 
ing paths  then  consists  of  the  columns  of  dioll,  tlie  direct  cerebellar 
tracts,  and  the  pyramidal  tracts,  and  Ave  must  now  attend  to  their 
longitudinal  distribution.  The  most  noticeable  feature  with  regard 
to  the  longitudinal  distribution  of  these  tracts  is  that  all  of  them 
increase  steadily  in  size  from  below  upwards,  thus  showing  that 
they  must  be  regarded  as  conducting  paths  between  the  central  gray 
tube  and  the  higher  ganglia.  It  is  impossible,  within  the  limits 
of  this  work,  to  describe  in  detail  the  encephalo-spinal  conducting 
paths,  but  a  general  view  of  their  course  and  connections  may  be 
obtained  from  the  annexed  diagrams.  These  paths  may  be  divided 
into  (1)  the  cerebro-spinal  and  (2)  cerebello-spinal  conducting  paths. 


E  N  C  E  P  H  A  L  0  -  S  P I N  O  -  N  E  U  R  A  r .    SYSTEM 


59 


Diagram  of  the  Gray  ^Masses  of  the  Simnal  Cord  and  Brain,  showinc  the  course  of  Tiir. 
Conducting  Paths     (After  Flechsig.) 
i?,  Fissure  of  Eolaiulo 
P"  P,  Tand  Pt,  Course  of  the  fibres  of  the  pyraiiiiilal  tract  from  their  origin  in  the  central  convolutions 

to  their  termination  in  the  anterior  gray  liorns  (a,  a'). 
I,   IT,  III,  First,   second,    and   third   portions  of  the   lenticular   nucleus   (NL).     NC,  Caudate   nucleus. 

Th,  Optic  thalamus. 
D,  O,  B,  A,  Points  from  which  fibres  issue  connecting  the  cortex  of  the  brain  and  basal  ganglion,  and 

also  the  gray  substance  of  the  pons  {PO}      Bd,  Fibres  connecting  the  cerebellum  and  optic  thalamus  ; 

and  Ottji,  those  connecting  the  cerebellum  and  the  gray  substance  of  tlie  pons. 
aq,  and  pq,  Anterior  and  posterior  pair  of  corpora  (juadrigemina  respectively. 
X,  Upper,  and  x',  lower  fibres  connecting  the  olivary  body  and  the  corpora  quadrigemina. 
FR,  Formatio  reticularis  of  the  medulla  oblongata,  formed  by  fibres  from  the  optic  thalamus  (Th),  the 

internal  division  of  the  inferior  peduncle  of  the  cerebellum  Hep),  from  the  spinal  cord  (/r,  ar,  and  ar'), 

and  probably  also  from  the  clavate  nucleus  (Nc). 
0,  Olivary  body ;   ecp,  fibres  of  the   restiforni   bodies  connecting  the   olivary   bodies  and   cirebcUum  ; 

other  fibres  connect  it  with  the  triangular  (Npr)  and  clavate  (Nc)  nuclei. 
dp,  Decussation  of  the  pyramids. 
pr',  Fibres  of  the  posterior  roots  whicli  pass  upwards  and  downwards  into  the  gray  substance,  and  pursue 

only  a  short  course. 
a,  a',  a",  a'",  anterior  roots. 
p,  pr,  pr",  O,  Fibres  of  the  posterior  roots 


60 


ANATOMICAL    IXTRODUCTION 


(1)   The  Cerebrospinal  Conducting   Paths. 
The  cereljro-spinal   contlucting  paths   are  represented   in   Figs.    32 

and  36. 

{a)  The  Pyramidal  Tract  (Fig.  32,  5,  5,  m).— The  fibres  of  this  tract 
issue  from  the  gray  matter  of  the  central  convolutions  of  the  brain, 


DiAGUAM  OF  Transverse  Section  of  the  Spinal  Cord  in  cppek  iiai.k  of  the  Dorsai,  Re(;ion. 

(After  Flechsii;.) 
C,  Anterior  commissure. 

dc'.  Fibres  which  pass  from  the  vesiculur  column  of  Clarke  (cc)  to  the  flirect  cerebellar  tract. 
P,  Posterior  horn . 

Figs.  Si;  ami  37. — Letters  cuminon  to  both. 
I't,  Pyramidal  tract  of  the  lateral  column. 
T,  Columns  of  Tiirck. 
dc,  Direct  cerebellar  tract. 
«r,  Internal  portion  of  the  anterior  root-zone. 
ar',  External  portion  of  the  anterior  root-zone. 
pr.  Posterior  root-zone. 
fi,  CJoir.s  columns. 

/)•,  Reticular  formation  of  the  spinal  cord. 
(I,  Anterior  gray  horns  of  the  spinal  cord. 

the  axis-cylinder  processes  of  the  giant  cells  already  described  being 
continuous  with  the  axis-cylinder  of  the  fibres  of  this  tract.  These 
fibres  form  at  first  more  or  less  separate  bundles,  which  descend  in  the 
centrum  semiovale  of  the  hemisphere,  and  come  together  on  reaching 


EXCEPHALO-SPIXO-XEURAL    SYSTEM. 


(U 


the  basal  ganglia  to  form  a  bundle,  ^vhich  occupies  the  anterior  t^vo- 
thirds  of  the  posterior  segment  of  the  internal  capsule.     The  fibres  lie 


Fig.  38. 


DiAljRAM    OF^THE   SPIXAL   SEGMENT   AS    A    CeNTKE   AM)   COXDVCTIXG   MedUM        (After  BrAMWELL  ) 

B,  right,  and  B',  left  liemispheres  of  the  brain ;  M  0,  lower  end  of  the  medulla  oblongata ;  1,  the 
niotor  tract  from  the  right  hemisphere  ;  it  divides  at  M  0,  and  the  larger  portion  crosses  over  to  the  oppo- 
site side  and  passing  down  the  lateral  column  it  supplies  the  muscles  M  and  M'  on  the  left  side  of  the 
body.  The  supply  to  HI  is  given  off  at  1'.  The  smaller  portion  passes  down  the  anterior  column  of 
the  same  side,  and  supplies  the  muscles  m  and  m'  on  the  right  side  of  the  body  ;  2,  the  motor  tract  on 
the  left  side  of  the  body  ;  the  larger  portion  crosses  over  to  the  opposite  side  and  supplies  the  mus- 
cles yi-  and  313  on  the  right  side  of  the  body,  wliile  the  lesser  portion  i>asses  down  the  same  side  and 
supplies  the  muscles  m^  and  m^  on  the  left  side  of  the  body  S,  S',  sensory  areas  on  the  left  side  of  the 
body  ;  3',  3,  the  main  sensory  tract  from  the  left  side  of  body ;  it  passes  up  on  the  opposite  side  (right)  of 
the  cord  in  the  postero-external  column,  and  proceeds  to  the  right  hemisphere  of  the  biain ;  S-,  S^,  sensoi'y 
areas  of  the  right  side  of  the  body ;  •!',  4,  the  main  sensory  tract  from  the  right  side  of  the  body,  proceed- 
ing up  the  left  side  of  the  cord  to  the  left  hemisphere  of  tlie  brain  The  arrow;^  indicate  the  direction  of 
the  conductiim. 


between  the  caudate  nucleus  and  optic  thalamus  on  the  inner,  and  the 
lenticular  nucleus  on  the  outer  side,  but  without  forming  any  connec- 


62  ANATOMICAL    INTRODUCTION. 

tions  with  these  ganglia,  and  pass  still  as  one  bundle  through  the 
middle  third  of  the  crusta  of  the  crus  cerebri.  On  reaching  the  pons 
the  fibres  become  separated  into  several  bundles  by  the  transverse  fibres 
of  the  middle  peduncle  of  the  cerebellum,  but  on  reaching  the  medulla 
oblono-ata  they  come  together  again  and  form  the  anterior  pyramid  of 
the  medulla,  and  it  is  from  this  circumstance  that  they  are  named  the 
pyramidal  tracts.  At  the  lower  end  of  the  medulla  by  far  the  largest 
portion  of  the  anterior  pyramid  crosses  over  to  the  lateral  column  of 
the  opposite  side  after  decussating  with  the  corresponding  fibres  of 
the  anterior  pyramid.  A  few  of  the  fibres  which  lie  on  the  external 
aspect  of  the  anterior  pyramid  pass  onwards  in  the  anterior  column  of 
the  spinal  cord  without  crossing,  and  these  form  the  columns  of  Tiirck. 

(b)  The  Sensory  Conducting  Paths. — The  fibres  of  the  posterior  nerve- 
root  diverge  like  a  fan  immediately  on  entering  the  spinal  cord  (Fig. 
37,  pr',  pr"),  and  most  if  not  all  of  them  cross  over  to  the  opposite 
side  (Fig.  38,  S  S'^),  and  then  ascend  to  reach  the  cerebral  cortex 
chiefly  of  the  occipital  and  temporo-sphenoidal  lobes.  The  course  of 
these  fibres  is  not  well  ascertained  at  all  the  intermediate  points. 
It  is  probable  that  in  the  spinal  cord  some  of  these  fibres  ascend  in 
the  posterior  gray  horn,  and  others  in  the  postero-external  column. 
Some  anatomists  believe  that  a  portion  of  the  sensory  conducting  path 
ascends  in  the  cord  on  the  same  side  as  the  root  from  which  it  is 
derived,  and  that  a  supplementary  decussation  of  sensory  fibres  takes 
place  in  the  medulla  oblongata  (Fig.  32,  S).  It  is,  however,  very 
doubtful  whether  such  a  supplementary  decussation  exists,  and  patho- 
logical observations  would  at  least  seem  to  indicate  that  the  sensory 
conducting  paths  belonging  to  the  opposite  side  of  the  body  pass 
through  the  restiform  body  of  the  medulla  oblongata.  These  fibres 
pass  upwards  in  posterior  and  external  bundles  of  the  longitudinal 
fibres  of  the  pons  and  come  together  to  form  one  bundle  in  the  ex- 
ternal third  of  the  crusta  (Fig.  32,  ps).  The  fibres  ascend  as  one 
bundle  on  the  posterior  third  of  the  posterior  segment  of  the  internal 
capsule,  and  at  this  point  they  are  joined  by  fibres  which  ascend  from 
the  optic  tracts  through  the  geniculate  bodies  and  anterior  tubercle  of 
the  corpora  of  the  quadrigemina  around  the  optic  radiations  of  Gratiolet, 
and  also  by  fibres  from  the  olfactory  tracts  of  the  opposite  side,  which 
reach  them  most  probably  through  the  anterior  commissure  of  the  third 
ventricle  and  the  optic  thalamus.  The  sensory  fibres  of  the  internal 
capsule  now  radiate  backwards,  outwards,  and  upwards  to  reach  the 
cortex  of  the  occipital  and  temporo-sphenoidal  lobes,  and  to  a  less 
extent  <lhat  of  the  parietal  lobe. 

The  connections  of  the  intermediate  ganglia  with  the  central  gray 


ENCEPIIALO-SPINO-NEURAL    SYSTEM.  C,;; 

tube  have  already  l)een  described,  and  tliest-  are  also  connected  with 
the  cortex  cerebri  by  fibres  whicli  ascend  in  the  corona  radiata. 

(2)    The  CerebeAlo-spinal   Conducting  Paths. 

(a)  The  Direct  Cerehellar  Tracts. — The  fibres  of  this  tract  appear 
to  take  their  origin  from  the  ganglion  cells  of  the  vesicular  column  of 
Clarke  (Fig.  -^7,  dr),  and  then  to  pass  out^vards  to  reach  the  surface 
of  the  lateral  column.  The  tract  makes  its  first  appearance  in  the 
upper  lumbar  or  lower  dorsal  region,  and  it  gradually  increases  in  size 
from  below  upwards,  by  the  addition  of  new  fibres.  It  lies  on  the 
surface  of  the  cord  to  the  outer  side  of  the  lateral  pyramidal  tract,  and 
on  reaching  the  medidla  oblongata  it  occupies  the  surface  of  the  resti- 
form  body  (Fig.  35,  dc\  and  finally  the  fibres  pass  through  the  in- 
ferior })eduncle  to  reach  the  cortex  of  the  cerebellum  (Fig.  38,  dc). 

{b)  The  Columns  of  GoU. — The  columns  of  Goll  begin  as  an  insig- 
nificant bundle  of  fibres  in  the  lumbar  region  of  the  cord,  and  gradually 
increase  in  size  from  below  upwards  (Fig,  35,  G).  The  inferior  origin 
of  the  fibres  is  not  well  ascertained,  but  it  is  probable  that  they  are 
directly  derived  from  the  jjosterior  roots.  On  reaching  the  medulla 
the  fibres  terminate  in  the  cells  of  the  clavate  nucleus  (Fig.  33,  en). 
This  nucleus  is  connected  l)y  arcuate  fibres  (Fig.  33,  10)  with  the  olivary 
body  of  the  same  side,  Avhich  in  its  turn  is  connected,  by  means  of  the 
inferior  peduncle  of  the  cerebellum,  with  the  cortex  of  the  cerebellum 
(Fig.  33,  7)  and  with  the  corpus  dentatum  (Fig.  33,  6)  of  the  opposite 
side.  The  interiHediate  (janglia  of  the  cerebeUo-spinal  system  are  con- 
nected with  one  another  and  with  the  cortex  of  the  cerebellum  in  vari- 
ous Avays.  The  transverse  fibres  of  the  middle  peduncle  of  the  cere- 
bellum (Fig.  33,  5)  connect  the  cortex  and  the  interposed  gray  matter  of 
the  pons  of  the  opposite  side  (Fig.  33,  P).  The  superior  peduncle 
contains  fibres  which  connect  the  cortex  (Fig.  33,  2)  and  the  corpus 
dentatum  (Fig.  33,  3)  with  the  red  nucleus  (Fig.  33,  R)  of  the  opposite 
side,  and  fibres  (Fig.  33,  1)  which  pass  near  the  red  nucleus  and  through 
the  optic  thalamus  to  connect  the  cortex  of  the  cerebellum  with  the 
cortex  of  the  opposite  hemisphere  of  the  brain. 

The  connections  of  the  cerebellar  system  with  the  anterior  gray 
horns  or  the  motor  part  of  the  spinal  cord,  are  not  well  ascertained, 
but  as  the  upward  continuation  of  the  anterior  root-zone  of  the  spinal 
cord  almost  surrounds  the  olivary  body  and  the  red  nucleus,  and  passes 
near  to  the  interposed  gray  matter  of  the  pons,  it  is  not  improbable  that 
connections  may  be  formed  between  them.  These  supposed  connec- 
tions are  represented  in  Fig.  33  by  the  lines  8,  8 ;   9,  9,  and  9''. 


CHAPTER  II. 

PHYSIOLOGICAL  INTRODUCTION. 

The  law  of  evolution  is,  as  the  student  has  already  learned,  as 
applicable  to  the  function  as  to  the  structure  of  the  nervous  S3^stem. 
It  is,  indeed,  manifest  that  there  must  be  a  determinate  relation  between 
these  two  factors  in  development.  The  most  general  expression  of 
this  relationship  is  that  unlike  functions  entail  unlike  structures  ;  and, 
inversely,  that  unlike  parts  assume  activities  of  unlike  kinds.  The 
whole  of  scientific  pathology  may  be  said  to  rest  upon  this  law,  for  we 
assume  that  deranged  nervous  functions  are  caused  by  disorders,  either 
molar  or  molecular,  of  nervous  structures  ;  and,  inversely,  that  injured 
or  diseased  nervous  structures  are,  or  were,  accompanied  by  correspond- 
ino-  disorders  of  nervous  functions.  In  tracing  the  development  of  the 
structure  of  the  nervous  system,  therefore,  it  was  found  impossible  to 
avoid  continual  reference  to  its  functions,  and  now  in  briefly  discussing 
the  functions  of  the  system  constant  reference  Avill  have  to  be  made  to 
its  structure. 

The  nervous  system  is,  as  we  have  seen,  composed  of  cells  and  fibres. 
The  cells  are  originators  of  motion,  and,  to  some  small  extent,  con- 
ductors also,  while  the  fibres  are  conductors,  and  only  in  a  very  small 
degree  originators  of  motion.  But  the  unit  of  composition  of  a  ner- 
vous system,  which  has  assumed  even  a  minor  degree  of  complication, 
is  a  cell  with  a  nerve  fibre  connecting  it  Avith  a  muscular  fibre  or  work 
organ,  or  a  cell  with  one  fibre  connecting  it  with  the  periphery  of 
the  body  and  another  with  a  muscular  fibre  or  work  organ.  In  the 
first  arrangement  the  cell  gives  out  energy  or  discharges  at  periodi- 
cal intervals,  and  the  liberated  energy  being  conducted  by  the  effer- 
ent fibres  to  the  work  organ,  gives  rise  to  rliythmical  contractions 
of  the  muscular  fibre.  This  constitutes  automatic  action.  In  the 
second  arrangement  an  impression  made  on  the  surface  of  the  body 
sets  up  a  disturbance  which  is  conducted  by  an  afferent  fibre  to  the 
nerve-cells,  where  it  liberates  a  store  of  energy  which  is  now  con- 
ducted outwards  to  the  muscular  fibre,  secreting  cell,  or  other  work 
organ.  This  constitutes  reflex  action.  Of  these  two  mechanisms,  the 
latter  is  by  far  the  most  important.  The  ganglia  and  strands  of  the 
sympathetic  system  appear  to  be  simply  an  aggregation  of  reflex  mech- 
anisms connected  together  in  various  ways,  and   Ave  shall,   therefore, 


SPINO-NEUEAL    SYSTEM.  05 

at  once  proceed  to  discuss  the  functions  of  the  spinal  and  encephalic 
systems. 


1.  FUNCTIONS  OF  THE  SPINO-NEURAL  SYSTEM. 

(1)  Reflex  Action.  —  The  ganglion  cells  of  the  anterior  gray 
horns  of  the  spinal  cord  are  centres  for  reflex  actions.  The  afferent 
fibres  of  the  reflex  loop  start  from  the  periphery  of  the  body  and  pass 
upwards  along  the  peripheral  nerves  and  through  the  posterior  roots 
and  posterior  gray  horns  to  join  the  ganglion  cells  of  the  anterior 
horns,  while  the  efferent  fibres  pass  outwards  through  the  anterior 
roots  and  peripheral  nerves  to  reach  the  muscles.  Two  forms  of  reflex 
action  maybe  distinguished,  {a)  the  superficial  and  (b)  the  deep  reflexes. 

(a)  The  superficial  reflexes  are  excited  by  stimulation  of  the  skin 
and  accessible  mucous  membranes. 

(b)  The  deep  reflexes  consist  of  muscular  contractions  evoked  bv 
striking  the  muscles  themselves,  stretching  their  tendons,  or  tapping 
certain  parts  of  the  periosteum,  and  probably  some  of  the  fascise. 
Some  physiologists  believe  that  the  tendon  reactions  are  caused  not  by 
reflex,  but  by  direct  action,  being  supposed  to  be  due  to  the  sudden 
stretching  of  the  muscular  substance  itself.  It  is,  however,  admitted 
by  all  that  the  integrity  of  the  reflex  loop  is  necessary  for  the  jn'oduc- 
tion  of  these  reactions,  and  we  shall  consequently  speak  of  them  in 
these  pages  as  if  they  were  proved  to  be  of  reflex  origin.  The  various 
forms  of  the  superficial  and  deep  reflexes  will  be  described  in  detail 
when  the  disorders  of  the  reflex  functions  are  under  consideration. 

(2)  Automatic  Actioji. — The  spinal  cord  contains  a  considerable 
number  of  what  have  been  regarded  as  automatic  centres,  but  it  is 
probable  that  many  of  them  act  in  a  reflex  manner.  The  lumbar 
portion  of  the  cord  contains  centres  for  the  regulation  of  the  acts  con- 
nected with  micturition,  defecation,  erection  and  ejaculation,  and  par- 
turition. The  medulla  oblongata  contains  numerous  centres  which  are 
more  or  less  automatic  in  their  actions.  The  following  may  be  men- 
tioned :  (a)  the  respiratory  centre,  {b)  the  cardiac  centre,  (c)  the  vaso- 
motor centre,  [d)  the  diabetic  centre,  or  more  probably  a  centre  for  the 
regulation  of  the  nutrition  of  the  liver  and  the  other  abdominal  viscera, 
(e)  the  centre  for  deglutition,  (/)  the  centre  for  the  movements  of  the 
stomach  and  oesophagus,  {g)  the  centre  for  the  regulation  of  the  secre- 
tion of  saliva,  and  (A)  the  centre  for  the  dilation  of  the  pupil. 

(3)  Tropliic  Functions  of  the  Cord. — The  ganglion  cells  of  the 
anterior  horns  exercise  a  trophic  influence  on  the  muscles  with  which 
thev  are  connected  bv  efferent  fibres.     It  is  also  probable  tliat  these 


66 


PHYSIOLOGICAL    INTRODUCTION. 


cells  exercise  a  controlling  influence  upon  the  nutrition  of  the  bones 
and  j(.ints,  while  the  cells  of  the  posterior  gray  horns  constitute  trophic 
centres  for  the  skin  and  its  appendages. 

(4)  Vaso-motor  and  Secretory  Functions. — Vaso-motor  centres  exist 
in  the  cord,  by  means  of  which  tonus  of  the  muscular  coat  of  the 
vessels  is  maintained.  The  secretions  of  the  glands  are  also  controlled 
by  the  spinal  centres,  and  the  peristaltic  movements  of  the  oesophagus, 
stomach,  and  intestines  are  regulated  from  the  cephalic  end  of  the 
central  o-ray  tube.     Little  is  known,  beyond  conjecture,  of  the  localiza- 


FiG.  39 

/■!■    3  3      2  1 

It  t   t  u 


X  A 

Diagram  of  the  Course  of  the  Peixiipal  Condvctinh  Paths  within  the  Cord.  (Aftor  Erh.  i 
1  and  1',  The  motor  and  vaso-motor  tracts  passing  througli  the  anterior  root  («),  and  remaining  on  tlie 
same  side  of  the  cord ;  2  and  2',  Tracts  which  conduct  the  muscular  sensibility,  also  passing  thruugh  the 
anterior  roots,  and  remaining  oh  the  same  side  of  the  cord  ;  3  and  ',i',  The  tracts  which  conduct  sensory 
impressions  of  touch,  temperature,  pain,  and  tickling.  These  enter  the  cord  through  the  posterior  roots, 
and  cross  to  the  other  side,  and  pursue  their  course  upwards  on  that  side.  Section  of  the  right  half  of  the 
cord  {«)  must  interrupt  conduction  through  the  motor,  vaso-motor,  and  musculo-sensory  tracts  (1  and  2) 
on  the  right  side,  and  the  cutaneous  sensory  tracts  on  the  left  side  (3'). 


tion  in  the  cord  of  the  centres  of  visceral  innervation.  That  they  are 
not  situated  in  the  anterior  gray  horns  is  rendered  certain  by  the  fiict 
that  the  visceral  movements,  and  the  automatic  actions  of  defecation, 
micturition,  erection,  and  parturition,  are  unaffected  in  those  diseases 
in  which  the  lesion  is  limited  to  the  anterior  gray  horns.  The  vesicu- 
lar column  of  Clarke,  the  ganglion  cells  of  which  are  bipolar  like  those 
of  the  sympathetic  ganglia,  may  possibly  contain  the  centres  of  visceral 
innervation. 

(5)  Fmictions  of  the~  Cerebrospinal  Conducting  Paths. — A  trans- 
verse lesion  of  the  cord,  if  complete,  gives  rise  to  loss  of  sensation  and 


ENCEPHALO-SPINAL    SYSTEM.  67 

voluntarv  motion  in  all  parts  of  the  body  which  are  innervated  from 
the  i)art  of  the  cord  which  is  below  the  level  of  this  disease.  If  the 
lesion  is  limited  to  one  lateral  half  of  the  cord,  the  sensations  of  touch, 
pain,  temperature,  and  tickling  are  lost  on  the  opposite  side  to  the 
disease,  while  muscular  sense  and  voluntar}^  motion  are  lost  on  the  same 
side.  The  annexed  diagram  (Fig.  39)  will  afford  a  sufficient  explana- 
tion of  this  statement. 

((J)  Functions  of  the  Cerehello-spinal  Conducting  Paths. — A  trans- 
verse lesion  of  the  spinal  cord  must  doubtless  arrest  conduction  through 
the  cerebellar  spinal  conducting  paths,  but  the  symptoms  which  might  be 
caused  by  injury  of  these  paths  are  altogether  obscured  by  the  presence 
of  voluntary  paralysis.  The  cerebellar  afferent  conducting  paths  are, 
however,  most  probably  interfered  with  when  the  posterior  columns  of 
the  cord  are  separately  diseased,  and  it  is  probable  that  the  incoordina- 
tion of  movements,  to  be  subsequently  described  under  the  name  of 
ataxia,  is  caused  by  injury  of  these  paths.  Disease  of  the  cerebello- 
spinal efferent  conducting  paths  is  not  known  as  a  separate  affection. 

2.  FUNCTIONS  OF  THE  ENCEPHALO-SPINAL  SYSTEil. 

All  recent  researches  have,  in  my  opinion,  tended  to  confii-m  Mr. 
Herbert  Spencer's  hypothesis :  "•  That  the  cerebellum  is  an  organ  of 
doubly  compound  coordination  in  space,  while  the  cerebrum  is  an  organ 
of  doubly  compound  coordination  in  time."  According  to  this  theory, 
which  has  been  adopted  and  elaborated  by  Dr.  Hughlings  Jackson,  the 
cerebellum  regulates  the  muscular  contractions  necessary  for  the  main- 
tenance of  all  our  attitudes  in  space,  while  the  cerebrum  regulates  the 
contractions  necessary  to  effect  all  the  changes  of  attitude  which  are 
made  in  response  to  the  successive  impressions  made  upon  the  organism 
in  time.  Now,  so  long  as  a  particular  attitude  is  maintained  in  oppo- 
sition to  gravity  or  other  forces,  the  contractions  of  the  various  groups 
of  muscles  concerned  must  be  continuous  and  in  equilibrium  with  one 
another ;  Avhile  each  change  of  attitude  necessitates  the  overthrow  of 
this  equilibrium  by  the  contractions  of  some  groups  of  muscles  pre- 
ponderating over  those  of  others,  and  thus  change  of  attitude  involves 
alternate  muscular  contractions  and  relaxations.  Speaking  broadly, 
then,  the  cerebellum  regulates  continuous  or  tonic  muscular  contrac- 
tions, while  the  cerebrum  regulates  alternate  or  clonic  contractions.  It 
will  be  seen,  therefore,  that  every  compound  muscular  adjustment 
necessitates  the  cooperation  of  both  these  organs.  No  change  of  atti- 
tude can  be  effected  by  the  cerebrum  except  in  so  far  as  a  certain  atti- 
tude was  previously  maintained  by  the  cerebellum,  and  no  steady  move- 
ment can  be  produced  by  the  alternate  contractions  of  some  groups  of 


QS  PHYSIOLOGICAL    IXTR  ODUCTIOX. 

muscles  except  in  so  far  as  other  groups  of  muscles  are  maintained  in 
a  state  of  continuous  contraction,  and  it  may  consequently  be  inferred 
that  all  the  movements  of  the  body  are  coordinated  both  in  the  cere- 
bellum and  cerebrum.  But  although  the  functions  of  the  cerebellum 
and  cerebrum  are  to  a  considerable  extent  coordinate,  yet  it  is  manifest 
that  the  former  must  act  in  subordination  to  the  latter. 

The  degree  of  development  to  which  an  animal  has  attained  may, 
indeed,  bemeasured  by  its  power  of  effecting  multitudinous  changes  of 
attitude,  and,  were  it  only  possessed  of  the  power  to  maintain  one  un- 
varying attitude,  its  degree  of  organization  would  not  require  to  be 
more  complicated  than  that  of  a  vegetable.  But,  in  effecting  these 
changes  of  attitude,  the  alternate  contractions,  under  the  guidance  of 
the  cerebrum,  must  take  the  lead,  and  any  change  Avhich  is  produced 
in  the  relative  strength  of  the  continuous  contractions,  although  regu- 
lated by  the  cerebellum,  must  be  in  strict  subordination  to  the  action 
of  the  cerebrum. 

3.  FUNCTIONS  OF  THE  CEREBRO-SriNAL  SYSTEM. 

The  central  gray  tube,  with  the  peripheral  nerves,  constitutes,  as  Ave 
have  seen,  a  system  of  simple  coordination  in  time  (reflex  action),  and 
Ave  must  noAv  point  out  that  the  basal  ganglia,  when  acting  upon  the 
central  gray  tube  and  peripheral  nerves,  form  a  system  of  compound 
coordination  in  time  (instinctive  action),  and  the  cortex  of  the  brain, 
when  acting  on  the  inferior  centres,  forms  a  system  of  doubly  compound 
coordination  in  time  (conscious  action).  Both  conscious  and  instinctive 
subconscious  movements  are  comprised  under  the  name  of  psychical 
actions.  Reflex  actions  consist,  as  Ave  have  seen,  of  three  factors  :  (a) 
conduction  to  a  nerve  centre  of  an  impression  made  on  the  surface ;  (b) 
reduction  to  order  of  these  impressions  in  the  centre ;  and  (e)  conduc- 
tion of  these  outwards,  with  ^  the  muscular  contractions  resulting  from 
them.  But,  as  has  been  frequently  stated  by  Mr.  Herbert  Spencer, 
four  factors  may  be  distinguished  in  every  psychical  action.  To  quote 
Mr.  Spencer's  own  language:  "  There  is  (a)  that  property  of  external 
objects  which  primarily  affects  the  organism — the  taste,  smell,  or 
opacity ;  and,  connected  Avith  such  property,  there  is  in  the  external 
object  that  character  (l>)  Avhich  renders  seizure  of  it  or  escape  from  it 
beneficial.  Within  the  organism  there  is  (c)  the  impression  or  sensa- 
tion Avhich  the  property  a  produces,  serving  as  stimulus,  and  there  is 
connected  Avith  it  the  motor  change  {d)  by  which  seizure  or  escape  is 
effected.  Now,  psychology  is  chiefly  concerned  <\ith  the  connection 
between  the  relation  ab  and  the  relation  cd,  under  all  those  forms 
which  they  assume  in  the  course  of  evolution.     Each  of  the  factors 


CEREBRO-SPINAL    SYSTEM".  69 

and  each  of  the  relations  grows  more  involved  as  organization  advances. 
Instead  of  being  single,  the  identifying  attribute  a  often  becomes,  in 
the  environment  of  a  superior  animal,  a  cluster  of  attributes,  such  as 
the  size,  form,  colors,  motions,  displayed  by  a  distant  creature  that  is 
dangerous.  The  factor  5,  with  which  this  distant  combination  of  attri- 
butes is  associated,  becomes  the  congeries  of  characters,  powers,  habits, 
which  constitute  it  an  enemy  of  the  subjective  factors ;  c  becomes  a 
complicated  set  of  visual  sensations  coordinated  with  one  another  and 
with  the  ideas  and  feelings  established  by  experience  of  such  enemies, 
and  constituting  the  motive  to  escape ;  while  d  becomes  the  intricate, 
and  often  prolonged,  series  of  runs,  leaps,  doubles,  dives,  etc.,  made  in 
eluding  the  enemy." 

The  account  first  given  of  reflex  and  psychical  action  shows  that  the 
former  consists  of  a  muscular  adjustment  made  in  response  to  ?l  pi-esent 
impression ;  while  the  latter  is  a  muscular  adjustment  excited  by  a 
present  impression,  but  made  to  attain  or  avoid  an  anticipated  impres- 
sion. In  reflex  action  the  muscular  adjustment  is  effected  by  means  of 
afferent  and  eff'erent  fibres  and  one  centre,  while  in  psychical  action  this 
mechanism  must  consist  of  at  least  afferent  and  efferent  fibres,  a  recep- 
tion and  an  emission  centre  with  some  means  of  intercentral  communi- 
cation. In  the  purely  unconscious  psychical  actions,  or  the  instinctive 
actions,  the  optic  thalamus  is  supposed  to  be  the  central  receptive  organ, 
and  the  corpus  striatum  the  central  emission  organ,  the  two  being  con- 
nected 1)7  white  fibres  which  interlace  with  the  longitudinal  filires  of  the 
internal  capsule.  The  cortex  of  the  cerebrum  with  its  afferent  and 
efferent  fibres  appears  to  be  the  organ  for  the  regulation  of  the  con- 
scious psychical  actions,  although  the  fact  that  individuals  sometimes 
sing  songs  or  recite  long  passages  of  poetry  during  the  unconscious 
stage  which  follows  an  epileptic  attack,  or  that  which  results  from  the 
mesmeric  state  or  from  chloroform  narcosis,  seems  to  show^  that  all  ac- 
tions, which,  like  spirits,  are  regulated  from  the  cortex  of  the  brain,  are 
not  necessarily  attended  by  consciousness.  A  glance  at  the  structure 
of  the  cortex  of  the  brain  (Fig.  30)  will  show  that  the  small  cells  of 
the  outer  layers  are  best  adapted  to  act  as  a  receptive  organ,  while  the 
caudate  cells  of  the  inner  layers  are  best  adapted  to  act  as  an  emissive 
centre.  The  structure  of  the  outer  layers  of  the  cortex  in  comparison 
with  the  inner  layers,  forcibly  reminds  one  of  the  structure  of  the  pos- 
terior gray  horn  of  the  spinal  cord  in  comparison  with  that  of  the 
anterior  horn.  In  the  outer  layers  of  the  cortex,  as  in  the  posterior 
gray  horn,  the  afferent  fibres  terminate  without  forming  definite  con- 
nections with  the  cells,  which  are  in  both  cases,  small,  round,  and  desti- 
tute of  processes,  while  in  the  inner  layers  of  the  cortex  and  in  the 


70  PHYSIOLOGICAL    INTEODUCTION . 

anterior  gray   horns,  the  cells,   which   are  large   and   furnished  with 
numerous  processes,  are  definitely  connected  with  the  axis-cylinders  of 

efferent  fibres. 

Now,  although  it  is  probable  that  the  outer  layers  of  the  cortex  of 
the  whole  cerebrum  constitute  a  receptive  organ,  and  the  inner  layers 
an  emissive  organ,  yet,  the  outer  layers  of  certain  districts  of  the  cortex 
have  become  specially  adapted  to  act  as  receptive  organs  or  sensory 
centres,  and  the  inner  layers  of  other  districts  have  become  specially 
adapted  to  act  as  emissive  organs  or  motor  centres. 

(1)  The  Sensory  Cortical  Centres. — From  his  first  experiment, 
Ferrier  concluded  that  the  centre  for  vision  was  situated  in  the  angular 
gyrus  and  surrounding  gray  matter;  the  auditory  centre  in  the  superior 
temporo-sphenoidal  convolution ;  the  centres  of  taste  and  smell  at  the 
extremity  of  the  temporo-sphenoidal  lobe,  and  that  of  touch  in  the 
uncinate  gyrus  and  the  hippocampus  major,  Munk  believes  that  the 
visual  centre  or  area  is  of  much  larger  extent  than  that  assigned  to  it 
by  Ferrier,  and  that  it  is  situated  in  the  occipital  lobes.  He  maintains 
that  removal  of  this  area  causes  Ijlindness,  and  that  extirpation  of  small 
portions  of  it  gives  rise  to  blindness  of  localized  areas  of  the  retina.  He 
beheves  that  there  are  three  visual  spheres  in  the  cortex  corresponding 
to  three  visual  areas  in  the  retina.  The  external  part  of  the  retina  of 
the  left  eye  is  connected  with  the  external  part  of  the  cortical  visual 
centre  in  the  left  hemisphere,  while  the  internal  and  central  portions  of 
the  retina  of  the  right  eye  are  respectively  connected  with  the  internal 
and  central  portions  of  the  visual  centre  of  the  left  or  opposite  hemi- 
sphere. The  upper  portion  of  the  retina  is  connected  with  tlie  front, 
and  the  lower  part  with  the  posterior  aspect  of  the  visual  centre  of  the 
opposite  hemisphere. 

Removal  of  both  visual  centres  causes,  according  to  Munk,  complete 
or  absolute  blindness,  while  partial  removal  of  these  areas  causes  incom- 
plete, or  what  Munk  calls  psycliical  blindness,  a  state  of  vision  first 
observed  by  Goltz,  in  which  the  animal  sees  and  avoids  objects,  but 
fails  to  recognize  the  special  properties  of  a  piece  of  meat,  for  example, 
which  renders  it  food  to  be  eaten  instead  of  an  obstacle  to  Ije  avoided. 
Munk  regards  the  whole  superior  and  internal  surface  of  the  cerebral 
hemisphere  as  constituting  a  sensory  area,  and  the  annexed  diagrams 
(Fig.  40)  indicate  the  manner  in  which  he  believes  these  centres  to  be 
distributed.  Very  elaborate  experiments  have  been  conducted  by  Drs. 
Ferrier  and  Yeo,  to  determine  the  exact  seat  of  the  centre  of  vision,  and 
the  most  important  conclusion  they  come  to  is  that  "  destruction  of  both 
angular  gyri  and  occipital  lobes  causes  total  and  permanent  blindness 
in  both  eyes  without  any  impairment  of  the  other  senses  or  of  motor 


CEREBRO-SPIXAL    SYSTEM.  71 

])Ower."  Blindness  or  heniiopia  Avas  caused  by  less  extensive  injuries, 
but  partial  or  complete  recovery  ahvays  ensued.  The  experiments  of 
Luciani  show  that  visual  disturbances  follow  extirpation,  not  only 
of  the  occipital,  but  also  of  the  parietal,  temporal,  and  frontal  lobes. 
It  may  therefore  be  concluded  that  the  localization  of  sensory  centres 
is  a  diffused  one,  and  that  the  whole  surface  of  the  cortex  is  possessed 
of  more  or  less  of  sensory  functions. 


Fig.  40. 


Upper  Sueface  of  the  Brain  of  the  Monkey.     (After  Munk.) 

Senxory  Areas :   A,  of  the  eyes;  B,  of  the  ears  ;  C,  of  the  sensibility  of  the  lower  extremitj' ;  D,  Anterior 

extremity  ;  E,  Head  ;  F,  Ocular  mu.scular  apparatus ;  G,  Region  of  ears  ;  H,  Neck ;  I,  Body. 

(2)  The  Motor  Qortical  Centres. — The  experiments  of  Hitzig  and 
Fritsch,  Terrier,  and  others  have  shown  that  stimulation  of  certain 
po'-tions  of  the  cortex  of  the  cerebral  hemispheres  by  electrical  currents 
is  followed  by  associated  muscular  movements  of  the  opposite  half  of  the 
body.  The  portion  of  the  cortex  which  is  thus  excitable  is  named  the 
motor  area.  This  area  corresponds  generally  with  the  ])art  supplied 
by  the  Sylvian  artery,  and  also  with  the  area  in  which  the  giant  cells, 
already  described,  have  been  discovered.  The  portions  of  the  cortex — 
the  areas  supplied  by  the  anterior  and  posterior  cerebral  arteries — which 
do  not  respond  to  electrical  excitation  are  called  latent  areas.  It  has 
also  been  found  that  extirpation  of  a  localized  portion  of  the  motor 
area  causes  paralysis  of  the  muscles  which  are  thrown  into  a  state  of 
spasm  by  electrical  excitation  of  this  portion.  The  annexed  diagrams 
(Figs.  41  and  42)  show  the  topographical  distribution  of  these  motor 
centres  on  the  outer  and  superior  surfaces  of  the  cerebral  hemispheres 
without  further  description.     The  experiments  of  Schafer  and  Horsley 


72  PHYSIOLOGICAL    INTRODUCTION. 

have  shoAvn  that  a  p(3rtion  of  the  cortex  of  the  internal  surface  of  the 
cerebral  hemisphere  is  excitable.  The  excitable  portion  is  limited  to 
the  marginal  convolution,  and  extends  as  far  forwards  as  the  junction 
of  the  middle  and  posterior  thirds  of  the  superior  frontal  convolution, 
and  as  for  backwards  as  a  point  opposite  the  centre  of  the  parietal 
lobule.  Speaking  in  general  terms,  stimulation  induces  contractions  of 
the  muscles  of  the  trunk  and  of  the  large  muscles  inserted  in  the 
j^houlder-blade  and  shoulder,  and  those  inserted  about  the  hip-joint. 

Fig.  41. 


Figs.  41  and  42.— Sihe  and  Upi'eu  Views  of  the  Bkain  of  Max.     (After  Ferkier  ) 
These  figui'es  are  constructed  by  marking  on  the  brain  of  man,  in  their  respective  situations,  the  motor 
areas  of  tlie  brain  of  the  monkey  as  determined  by  experiment,  and  the  description  of  the  effects  of  stimu- 
lating the  various  areas  refers  to  tlie  brain  of  the  monkey. 
1  (On  the  posterior-parietal  lob\ile\  Advance  of  the  opposite  hind  limb  as  in  walking. 
2,  3,  4  (Around  the  upper  extremity  of  the  fissure  of  Rolando),  Complex  movements  of  the  opposite  leg 

and  arm,  and  of  the  trunk  as  in  swimming, 
a,  6,  c,  d  (On  the  ascending  parietal  convolution).  Individual  and  combined  movements  of  the  fingers 

and  wrist  of  the  opposite  hand.     Prehensile  movements, 
o  (At  the  posterior  extremity  of  the  superior  frontal  convolution\  Extension  forward  of  the  opposite 

arm  and  hand. 

6  (On  the  upper  part  of  the  ascending  frontal  convolution).   Supination  and  flexion  of  the  opposite 

forearm. 

7  (On  the  median  portion  of  the  ascending  frontal  convolution  >,  Retraction  and  elevation  of  the  oppo- 

site angle  of  the  mouth  by  means  of  the  zygomatic  muscles. 

8  (Lower  down  on  the  same  convolution),  Elevation  of  the  ala  nasi  and  upjier  lip  with  depression  of 

the  lower  lip  on  the  opposite  side 


C  E  R  E  1 5  R  0  -  S  P I N  A  L    S  Y  S  T  E  :N[  . 


rs 


(o)  Tlw  Intireentral  Connections. — The  central  ends  of  the  indi- 
vidual sensory  mechanisms  are  unified  'bf  a  collective  centre — the  sen- 
sormm  commune — which  is  the  general  centre  of  nervous  connections 
on  the  afferent  side.  It  may  also  be  supposed  that  the  individual 
motor  centres  are  unified  by  a  general  centre  of  nervous  connections 
which  may  be  regarded  as  a  motorium  commune.     Between  the  sen- 


FiG.  42. 


0,  10  (At  the  inferior  extremity  of  the  ascending  frontal  and  posterior  extremity  of  the  third  frontal 
convolution),  Opening  of  the  mouth  with  (9)  protrusion  and  (10)  retraction  of  the  tongue. 
Region  of  Aphasiu. 

11  (At  the  inferior  extremity  of  the  ascending  parietal  convolution),  Eetraction  of  the  opposite  angle 

of  the  mouth,  the  head  turned  slightly  to  one  side. 

12  (On  the  posterior  portions  of  the  superior  and  middle  frontal  convolutions),  Eyes  opening  widely, 

pupils  dilating,  and  the  head  and  eyes  turning  towards  the  opposite  side 
13,  13'  (On  the  supramarginal  lobule  and  angular  gyrus).  The  eyes  moving  towards  the  opposite  side- 

with  an  upward  (13;  or  downward  (13')  deviation.     Pupils  generally  contracting.     (Centre  of 

Vision.) 
14  (On  the  inframarginal  or  superior  temporo-.sphenoidal  convolution),  Pricking  up  of  the  opposite  ear, 

head  and  eyes  turning  to  the  opposite  side,  and  pupils  dilating  largely.     (Centre  of  hearing.) 
Ferrier,  moreover,  places  the  centres  of  taste  and  smell  at  the  extremity  of  the  temporo-sphenoidiil 

lobe,  and  that  of  touch  in  the  gyrus  uncinatus  and  hippocampus  major. 


74  PHYSIOLOGICAL    INTRODUCTIOX . 

sorium  commune  and  the  motorium  commune  there  is  no  distinct  line 
of  demarcation,  nor  is  there  any  definite  boundary  between  these 
hio-hest  centres  and  the  individual  sensory  and  motor  centres.  All  of 
them  run  indistinguishably  into  one  another,  and  all  of  them  are  rep- 
resented bv  the  cortex.  The  activity  of  the  individual  sensory  centres 
is  the  con-elation  of  sensation  and  feeling,  and  of  the  highest  sensory 
centre  of  perception — emotion,  and  the  highest  operation  of  the  intel- 
lect, while  the  activity  of  the  motor  centres  is  the  correlation  of  con- 
scious exertion  and  the  will.  But  although  the  molecular  activity  of 
the  cortex  of  the  brain  is  the  correlative  of  consciousness,  all  parts  of 
the  cortex  do  not  stand  in  e(iual  relation  with  feeling.  It  seems  to  me 
that  consciousness  is  correlated  in  a  special  manner  with  the  activity  of 
the  small  cells,  which  are  destitute  of  processes  and  definite  connections. 
When  an  unaccustomed  impression  is  made  upon  the  surface  of  the 
body  the  impulses  are  conducted  inwards  to  the  small  cells  of  the  outer 
layers  of  the  cortex,  and  the  energy  set  free  by  the  unusual  disturbance 
is  in  great  part  expended  in  producing  a  new  organization  amongst  these 
cells,  and  it  is  during  the  progress  of  this  organization  that  psychical 
action  is  attended  by  the  highest  consciousness.  But  in  proportion  as 
this  impression  becomes  frequently  repeated  in  experience,  the  organi- 
zation of  the  cells  becomes  more  and  more  complete  by  the  establish- 
ment of  new  connections,  and  after  a  time  the  channels  of  communica- 
tion between  the  receptive  and  emissive  organs  become  so  open  that  the 
muscular  adjustment  follows  the  impression  promptly  and  in  almost  a 
wholly  unconscious  manner.  The  degree  of  consciousness  which 
attends  a  particular  operation  may,  therefore,  be  regarded  as  an  expres- 
sive indication  of  the  resistance  offered  to  the  molecular  movements  or 
impulses  in  passing  from  the  central  receptive  to  the  central  emissive 
organs.  Nor  is  this  all.  It  is  very  probable  that  the  part  of  the 
centre  which  is  most  remote  from  both  the  sensory  and  motor  centres 
will,  durintr  its  activity  be  correlated  with  the  highest  consciousness. 
This  part  is  what  is  called  the  praefrontal  area  of  the  coi'tex,  and  the 
fact  that  consciousness  is  lost  at  a  much  earlier  period  in  epileptiform 
attacks  caused  by  lesions  of  this  area  than  in  the  attacks  which  are 
caused  by  lesions  in  other  areas  of  the  cortex,  speaks  much  in  favor  of 
the  supposition  just  advanced. 

The  different  cortical  sensory  and  motor  centres  are  connected  with 
one  another  in  various  ways  by  systems  of  white  fibres.  These  SA'stems 
are  the  longitudinal  or  collateral  fibres,  consisting  of  the  arcuate  fibres 
or  fibrse  proprise,  fibres  of  the  gyrus  fornicatus,  longitudinal  septal  fibres, 
tlie  fasciculus  uncinatus,  the  longitudinal  inferior  fasciculus,  the  longi- 
tudinal fibres  of  the  corpus  callosum,  and   the  perpendicular  occipital 


CEREBELLO-SPINAL    SYSTEM.  75 

fasciculus  described  by  Wernicke,  and  the  transverse  or  commissural 
fibres,  wliicli  connect  similar  points  of  the  convolutions  of  the  two 
hemispheres,  and  which  consist  of  the  transverse  fibres  of  the  corpus 
callosum,  and  the  fibres  of  the  anterior  and  posterior  commissures  of 
the  third  ventricle. 


4.  FUNCTIONS  OF  THE  CEREBELLO-SPINAL  SYSTEM. 

The  cerebellum  must,  like  the  cerelirum,  act  on  the  muscular  svstem 
through  the  spinal  cord  and  peripheral  nerves.  The  central  gray  tube, 
as  we  have  seen,  forms  with  the  peripheral  nerves  a  system  of  simple 
coordination  in  time,  and  we  now  find  that  it  likewise  forms  a  system 
of  simple  coordination  in  space  (reflex  tonus) ;  the  intermediate  ganglia 
of  the  cerebello-spinal  system  acting  on  the  central  gray  tube  and 
peripheral  nerves  form  a  system  of  compound  coordination  in  space 
(maintenance  of  unvarying  attitudes),  and  the  cortex  of  the  cerebellum 
acting  on  the  inferior  centres  forms  a  system  of  doubly  compound 
coordination  in  space  (the  adjustment  of  the  tonic  contractions  of  the 
muscles  rendered  necessary  by  changes  of  attitude).  If  now  tlie  cere- 
bellum is  an  organ  for  producing  a  balanced  state  of  contraction  of  the 
muscles  in  the  maintenance  of  attitudes,  it  may  be  expected  that  injury 
of  this  organ  will  cause  a  loss  of  this  balance  and  a  conse(|uent  diffi- 
culty in  maintaining  complex  attitudes.  Flourens  was  the  first  to 
observe  the  effect  of  injuries  of  the  cerebellum  on  the  maintenance  of 
attitudes,  or  on  equilibration,  as  it  is  called.  He  found  that  when  a 
small  portion  of  the  cerebellum  was  removed  from  a  pigeon,  the  animal's 
gait  became  unsteady,  and  that  when  larger  portions  were  taken  away, 
the  movements  became  very  disorderly.  Experiments  on  animals  have 
also  shown  that  section  of  the  middle  peduncle  of  the  cerebellum  is 
followed  by  a  forced  movement  of  the  body  in  which  the  animal  rolls 
round  its  longitudinal  axis,  the  rotation  being  generally  towards  the 
side  operated  upon.  Injury  of  the  lateral  lobe  of  the  cerebellum,  and 
probably  of  the  fibres  of  the  peduncle  as  they  pass  transversely  through 
the  pons,  produces  the  same  kind  of  forced  moyeiaent  as  section  of  the 
middle  peduncle.  Nothnagel  concludes  from  experiments  on  rabbits 
that  lesions  which  injure  the  fibres  uniting  the  two  sides  of  the  organ 
occasion  the  greatest  amount  of  motor  disturbance.  Ferrier  found 
that  electrical  stimulation  of  the  cortex  of  the  cerel)ellum  in  animals 
caused  movements  of  both  eyes  with  associated  movements  of  the  head, 
limbs,  and  pupils.  Our  relations  to  the  external  objects  in  space  are 
largely  determined  by  the  sense  of  vision,  which  is  better  adapted  than 
any  of  the  other  senses  for  conducting  a  large  number  of  simultaneous 
impressions  from  the  periphery  to  the  centres,  and  it  may  consequently 


7(3 


PHYSIOLOGICAL    INTKODUCTION . 


be  expected  that  the  organs  of  vision  will  stand  in  a  peculiarly  intimate 
relation  to  the  chief  organ  for  regulating  the  attitudes  of  the  body. 
The  semicircular  canals,  with  the  portion  of  the  auditory  nerve  which 
supplies  them,  appear  to  form  a  special  peripheral  organ  for  determining 
the  attitudes  of  the  body  through  the  cerebellum. 


5.  COOPERATION  OF  THE  CEREBRO-SPINAL  AND  CEREBELLO- 
SPINAL SYSTEMS. 

According  to  the  theory  which  has  just  been  advanced  the  multitu- 
dinous adjustments  of  the  body,  both  in  time  and  space,  are  regulated  by 
the  combined  action  of  the  cerebrum  and  cerebellum  acting  through  the 
spinal  cord  and  peripheral  nerves.  The  cooperation  of  these  organs  in  the 
regulation  of  motor  actions  is,   however,  generally  of  an  antagonistic 

Fig.  43 


CL"  a'  a 

Schema  of  Encephalo-spixal  Action. 
8,  Motor  ganglion  cell  of  spinal  cord  ;  c,  Ganglion  chH  of  cortex  of  cerebrum,  and  d ,  of  cortex  of  cere- 
bellum ;  o,  o',  a",  Afferent  fibres  to  the  spinal  cord,  and  to  the  cortices  of  the  cerebrum  and  of  the  cere- 
bellum respectively ;  e,  e,  Efferent  fibres  from  the  spinal  ganglion  cell  to  m,  »n',  the  muscles  ;  e'  and  e", 
Fibres  from  the  cerebral  and  cerebellar  cells  respectively  to  the  spinal  ganglion  cell ;  i,  Intercentral  filire 
connecting  the  cerebral  and  cerebellar  cells.     The  arrows  indicate  the  direction  of  the  conduction. 

kind.  The  cerebellum  tends  to  maintain  an  unvarying  attitude,  Avhile 
the  cerebrum,  in  initiating  a  change  of  attitude,  must  act  by  overthrowing 
the  balance  of  the  muscular  contractions  which  maintain  this  attitude. 
The  overthrow  of  this  eciuilibrium  can  Ije  effected  by  the  cerebrum  in 


CEREBKO-SriNAL    AXD    CE  R  E  BE  LLO  -  SP  IX  AL    SYSTEMS.       77 

either  of  two  ways,  either  positively  by  an  increase  of  nervous  impulses 
to  certain  groups  of  muscles,  or  negatively  by  arresting  or  inhibitino-  in 
the  spinal  centres  the  cerebellar  influx  to  their  antagonists.  Now  it  is 
manifest  that  the  latter  method  would  be  much  more  economical  than 
the  former,  and  consec^uently  there  is  every  reason  to  believe  that  the 
cerebrum  does  act  largely  by  inhibiting  the  action  of  the  cerebellum, 
although  it  is  also  certain  that  it  must  exercise  a  positive  control  over 
the  various  muscular  contractions.  The  conjoint  action  of  the  central 
gray  tube,  the  cerebrum,  and  cerebellum  is  represented  in  the  accom- 
panying diagram  (Fig.  43)  under  the  simplest  conditions.  A  ganglion 
cell  of  the  spinal  cord  is  represented  by  s,  of  the  cerebrum  by  c,  of 
the  cerebellum  by  c'.  The  afferent  conducting  paths  from  the  periphery 
to  the  spinal  cord,  cerebrum,  and  cerebellum  are  represented  by  a,  a\  a" 
respectively.  The  efferent  conducting  path  between  the  cerebrum  and 
spinal  cord  is  represented  by  e',  between  the  cerebellum  and  cord  by  e", 
and  lietween  the  cord  and  muscles  l)y  e,  while  m  m  represent  the  mus- 
cles themselves,  and  the  arrows  indicate  the  direction  of  the  currents. 
Now,  when  an  impression  is  made  upon  a,  it  is  conveyed  to  .s,  and 
reflected  through  e  e  to  m  m,  this  constituting  a  simple  reflex  action. 
When  an  impression  is  made  upon  a",  the  impulse  is  conveyed  to  c' 
and  through  e"  to  s,  and  through  e  e  to  m  m,  producing  a  continuous 
contraction  of  the  muscles.  But  when  an  impression  is  made  upon  a', 
an  impulse  is  conveyed  to  c  and  dowuAvards,  through  e  to  s.  Now,  the 
impulses  conveyed  through  e'  to  s  may  produce,  Avhen  of  a  certain 
degree  of  intensity,  only  an  arrestive  or  inhibitory  action  on  the  im- 
pulses conveyed  to  s  through  a  and  e",  while  an  additional  degree  of 
intensity  enables  it  to  pass  through  s  and  e  <?  to  m  m,  and  to  produce 
clonic  muscular  contractions.  It  is  also  probable  that  the  cerebrum 
may  exercise  both  an  inhibitory  and  excitative  action  on  the  cerebellum 
through  the  intercentral  fibres  (i),  which  connect  the  centres  directly 
with  each  other.  This  hypothesis  was  first  stated  by  Dr.  Hughlings 
Jackson,  and  he  has  since  applied  it,  with  his  usual  subtle  and  gen- 
eralizing power,  to  the  explanation  of  various  pathological  phenomena. 
As  this  is  an  exceedingly  important  theory,  it  Avill  be  as  well  to  illus- 
trate the  actions  of  the  cerebrum  and  cerebellum  by  reference  to  the 
muscular  contractions  necessary  for  the  maintenance  of  the  erect 
posture  and  for  locomotion. 

(a)  The  E^^ect  Posture. — In  the  erect  posture  the  weight  of  the  body 
is  borne  by  the  plantar  arches,  and  the  body  is  maintained  by  a  series  of 
muscular  contractions  in  such  a  position  that  the  line  of  gravity  falls 
within  the  area  of  the  feet.  In  this  position  the  line  of  gravity  of  the 
head  falls  in  front  of  the  occipital  articidation,  that  of  the  combined 


PHYSIOLOGICAL    INTRODUCTION. 


Fig.  44. 


Diagram  Illustrating  the 
Attachments  of  some  of  the 
MOST      Important      Muscles 

WHICH   KEEP  THE   BoDY  IN  THE 

Erect  Posture.    (After  Hux- 
ley.) 

I.  Muscles  of  the  Calf. 
II.  Those  of  the  back  of  the 
Thigh.  III.  Those  of  the 
Spine,  which  tend  to  keep  the 
body  from  falling  forwards. 
1,  the  Muscles  of  the  front  of 
the  Leg  ;  2,  those  of  the  front 
of  the  Thigh  ;  3,  those  of  the 
front  of  the  Abdomen  ;  4,  5, 
those  of  the  front  of  the  Neck, 
which  tend  to  keep  the  body 
from  falling  backwards.  The 
arrows  indicate  the  direction 
of  action  of  the  muscles,  the 
foot  being  fixed. 


head  and  trunk  passes  behind  a  hne  joining  the 
two  hip-joints,  that  of  the  com1)ined  head,  trunk, 
and  thighs  falls  a  little  behind  the  knee-joints, 
and  the  line  of  gravity  of  the  whole  body  passes 
in  front  of  the  line  drawn  between  the  two 
ankle-joints.  This  statement  of  the  direction  of 
the  line  of  gravity  shows  that  when  the  foot  is 
made  the  surface  of  support,  the  body  would 
fall  forwards  unless  prevented  by  contraction  of 
the  muscles  of  the  calf  (Fig.  44,  I).  "  But 
this  action,"  says  Prof.  Huxley,  "tends  to  bend 
the  leg,  and  to  neutralize  this  and  keep  the  leg 
straight  the  great  muscles  in  front  of  the  thigh 
(Fig.  44,  2)  must  come  into  play.  But  these, 
by  the  same  action,  tend  to  bend  the  body  for- 
ward on  the  legs ;  and  if  the  l)ody  is  to  be  kept 
straight  they  must  be  neutralized  by  the  action 
of  the  muscles  of  the  buttocks  and  of  the  back 
(Fig.  44,  III)."  It  will  be  seen,  however,  that 
since  the  centre  of  gravity  of  the  combined 
head  and  trunk  falls  a  little  behind  the  line 
joining  the  hi]>s,  the  muscles  of  the  buttocks, 
although  stronglv  contracted  in  effecting  the 
erect  position,  do  not  require  to  contract  in 
order  to  maintain  it. 

The  muscles  of  the  calf,  those  of  the  front  of 
the  thigh,  and  the  erector  spinne  are  therefore 
the  most  active  muscles  in  maintaining  the  erect 
posture,  and  these  are,  according  to  the  hypothe- 
sis, maintained  in  a  state  of  tonic  contraction, 
mainly  by  the  cerebellum. 

(b)  Walking. — At  each  step  in  w'alking  there 
is  a  moment  at  which  the  body  rests  vertically 
on  the  foot  of  one  leg  (say  the  right),  Avhich  is 
then  called  the  '■'■active  leg."  The  other  (left), 
which  is  now  called  the  ^'■passive  leg,"  is  at  this 
time  inclined  obli(^uely,  Avith  the  heel  raised  and 
the  toe  resting  on  the  ground.  The  left  leg, 
slightly  flexed  to  avoid  contact  with  the  ground, 
is  now  swung  forwards  like  a  pendulum,  the 
length  of  the  swing  or  step   being  determined 


CEREBRO-SPINAL    AND    CEEEBELLO  -  SPIN  AL    SYSTEMS.       79 

by  the  length  of  tlie  leg,  the  left  toe  is  brought  to  the  ground,  and  the 
step  is  finished.  The  left  leg,  Avhich  was  previously  passive,  now 
gradually  becomes  straight  and  rigid,  and  the  body  is  moved  forwards 
<»n  the  left  toe  as  a  fulcrum  ;  while  the  right  leg,  which  was  previously 
at-tive,  assumes  an  inclined  position,  with  the  heel  raised  and  the  toe 
resting  on  the  ground,  so  that  it  is  ready  to  swing  forwards,  and  then 
once  more  to  assume  the  role  of  activity,  while  its  fellow  becomes  in  its 
turn  passive  again.  During  the  forward  movement  the  centre  of 
gravity  of  the  body  describes  a  curve,  the  convexity  of  which  is  up- 
ward ;  hence  in  successive  steps  the  centre  of  gravity,  and  with  it  the 
{(>])  of  the  head,  describes  a  series  of  curves,  with  their  convexities 
upwards. 

In  standing  on  Ixjth  feet  the  line  of  gravity  falls  betAveen  them,  )jut 
in  walking  it  must  be  alternately  shifted  from  one  foot  to  the  other,  in 
order  to  balance  the  body  on  the  active  leg.  While  the  left  leg,  for 
instance,  is  passive  and  swinging,  the  line  of  gravity  falls  within  the 
area  of  the  right  foot,  and  passes  through  the  right  lateral  half  of  the 
pelvis,  and  as  the  left  foot  becomes  active  the  centre  of  gravity  is 
shifted  to  the  op])osite  side,  and  the  line  of  gravity  passes  through  the 
left  lateral  half  of  the  pelvis  to  the  left  foot.  In  walking,  therefore, 
the  centre  of  gravity  describes  not  only  a  series  of  vertical  but  also  a 
series  of  horizontal  curves,  so  that  the  curve  described  by  the  head  is 
composed  of  vertical  and  horizontal  factors.  In  slow  walking  there  is 
an  appreciable  time  during  which  both  feet  are  on  the  ground ;  the  one 
being  planted  so  as  to  become  active  before  the  other  has  ceased  its 
activity.  In  fast  walking  this  period  is  very  short,  the  one  leaving  the 
ground  the  moment  the  other  touches  it,  while  in  running  there  is  an 
interval  during  which  neither  foot  is  on  the  ground. 

Let  us  now  attend  to  the  muscles,  the  contraction  of  which  effects  the 
changes  of  attitude  necessarily  involved  in  walking.  Suppose  that  we 
start  with  the  right  leg  in  the  vertical  position,  with  the  line  of  gravity 
passing  within  the  line  of  the  right  foot,  and  the  left  partially  raised 
from  the  around.  The  first  indication  of  a  forward  movement  must  be 
eff"ected  by  a  contraction  of  the  flexors  of  the  foot  on  the  leg,  which, 
as  the  toe  is  fixed,  bends  the  leg  and  with  it  the  whole  body  forwards. 
This  contraction  fixes  the  upper  end  of  the  tibia,  the  leg  being  bent 
forwards  at  an  acute  angle  with  the  foot,  and  the  femur  is  kept  extended 
on  the  tibia  by  a  rigid  contraction  of  the  muscles  of  the  front  of  the 
thigh.  The  lower  end  of  the  femur  and  upper  end  of  the  tibia  are 
now  rendered  fixed  points,  the  line  of  gravity  is  rapidly  passing  forwards 
from  the  middle  of  the  foot  to  the  toe,  the  weight  is  thus  taken  off"  the 
heel,  and  contraction  of  the  muscles  of  the  calf  causes  its  elevation. 


}iO  PHYSIOLOGICAL    IXTRODUCTIOX. 

But  tlie  line  of  gravity  is  now  passing  through  the  toe,  in  front  of  the 
knee,  and  in  front  of  the  centre  of  the  hip-joint,  so  that  the  muscles  of 
the  back  of  the  thigh  and  those  of  the  buttocks  must  contract  strongly 
or  the  body  would  be  flexed  on  the  thighs,  while  the  erectors  of  the 
spine  must  be  sufficiently  contracted  to  keep  the  different  segments  of 
the  body  in  a  rigid  condition.  It  is  manifest  that  as  soon  as  the  line 
of  p-ravity  passes  in  front  of  the  centre  of  the  hip-joint  and  through 
the  toe,  although  muscular  action  may  maintain  the  different  segments 
of  the  body  extended,  no  muscular  action  can  prevent  the  body  as  a 
whole  from  falling  forwards  on  the  toe  as  a  pivot,  and  the  body  would 
fall  unless  the  left  foot  were  now  in  a  position  to  be  planted  on  the 
o-round  in  front  of  the  line  of  gravity,  and  ready  to  assume  the  role  of 
the  active  leg.  Before,  however,  the  left  leg  can  become  active,  the 
line  of  gravity  must  be  transferred  to  the  left  foot,  and  before  the  right 
foot  can  be  made  to  swing  it  must  be  shortened  so  as  to  avoid  contact 
with  the  ground.  These  operations  are  so  im])ortant  as  to  require  care- 
ful study. 

(c)  The  transference  of  the  centre  of  gravity  from  the  passive  to 
the  active  leg  is  largely  effected  by  the  contraction  of  the  abductors  of 
the  thigh,  especially  by  the  gluteus  medius,  contraction  of  which,  the 
left  thigh  being  fixed,  causes  the  pelvis  to  rotate  vertically  on  the  hip- 
joint;  so  that  the  centre  of  gravity,  and  with  it  the  head,  describes 
a  curve  to  the  left,  with  its  convexity  upAvards,  a  movement  which  at 
the  same  time  slightly  elevates  the  pelvis  and  Avith  it  the  hip-joint  of 
the  opposite  side.  The  slight  elevation  of  the  right  hip-joint  not  only 
transfers  the  centre  of  gravity  to  the  left,  but  also  increases  the  distance 
of  the  centre  of  movement  (hip-joint)  of  the  passive  leg  (right)  from 
the  ground,  and  thus  prepares  for  the  forward  SAvinging  of  the  right 
leg.  The  contraction  of  the  abductors  is  accompanied  by  a  contraction 
of  their  antagonists — the  adductors,  Avhich  not  only  gives  steadiness  to 
the  pelvis  but  holds  the  latter  in  I'eadiness  to  counteract  at  once  any 
tendency  to  overaction  on  the  part  of  the  former,  by  Avhich  the  line  of 
gravity  Avould  be  carried  beyond  the  middle  of  the  foot.  The  curve 
described  by  the  head  OAving  to  contraction  of  these  muscles  Avould 
indeed  be  much  greater  than  \l  is  Avere  it  not  compensated  by  contrac- 
tion of  other  muscles.  At  the  time  that  the  abductors  of  the  left  leg  con- 
tract, and  thus  rotate  the  pelvis,  the  centre  of  gravity,  and  head  to  the 
left,  the  erector  spinee  of  the  right  side  enter  into  a  somcAvhat  additional 
contraction  producing  a  compensating  curve  to  the  right,  so  that  the 
head  does  not  deviate  to  the  left  during  the  transference  of  the  centre 
of  gravity  to  the  left  foot  to  anything  like  the  extent  that  might  l)e 
expected. 


CEEEHRO-SPIXAL    AXD    C  E  1!  E  15ELL0  -  S  ]' 1  X  AL    SYSTEMS.       bl 

(d)  Sivinginti  of  the  Passive  Leg. — It  lias  just  been  said  tliat  Avlien 
the  left  leg  becomes  active  the  pelvis  rotates  vertically  on  the  left  hip, 
so  that  the  opposite  hip-joint  is  slightly  elevated  to  an  extent  sufficient 
to  take  the  weight  of  the  body  from  the  right  toe,  but  inasmuch  as  the 
right  foot  is,  at  the  time  it  is  about  to  become  passive,  extended  ob- 
liquely, with  the  toe  depressed,  while  the  left  is  placed  nearly  vertically, 
the  former  is  much  too  long  to  swing  past  the  other  without  touchino- 
the  ground,  and  the  slight  vertical  rotation  of  the  pelvis  just  described 
does  not  give  the  requisite  elevation  for  this  purpose.  In  order  to 
swing  forwards,  therefore,  the  right  leg  is  still  further  shortened  bv 
flexion  of  its  various  segments  on  the  body  and  on  one  another.  The 
thigh  is  slightly  flexed  on  the  body,  the  leg  on  the  thigh,  and  the  foot 
on  the  leg.  Of  these  movements  the  slight  elevation  of  the  toe  caused 
by  dorsal  flexion  of  the  foot  is  by  far  the  most  important  and  special ; 
it  is  this  movement  which  distinguishes  the  walk  of  the  adult  from  that 
of  the  infant,  the  latter  advancing  the  passive  foot  not  by  a  pendulum 
motion,  but  by  a  voluntary  eifort  in  which  the  leg  and  foot  are  raised 
from  the  ground  by  the  flexion  of  the  thigh  on  the  body.  It  may  also 
be  mentioned  that  the  adductors  of  the  thigh  manifest  a  very  special 
action  in  assisting  to  cross  one  leg  over  the  other — an  action  which 
cannot  be  effected  by  the  lower  animals,  or  by  the  human  inflint,  and 
hence  these  muscles  must  also  be  regarded  as  being  in  an  esjiecial 
manner  under  cerebral  influence.  The  cerebro-spinal  influence  is 
therefore  manifested  in  the  active  leg  during  locomotion  by  securino-  a 
strong  contraction  of  the  anterior  flexors  of  the  foot,  and  of  the  flexors  of 
the  leg  on  the  thigh  along  with  the  abductors  so  as  to  fix  and  rotate  the 
pelvis  vertically,  while  it  is  manifested  in  the  passive  leg  partly  by  con- 
traction of  the  flexors  of  the  thigh  on  the  body,  partly  by  contraction 
of  the  flexors  of  the  leg  on  the  thigh,  and  partly  by  flexion  of  the  foot 
on  the  leg,  the  flexion  in  all  these  instances  being  ])robably  due  less  to 
active  contraction  than  to  relaxation  of  the  antagonistic  muscles.  The 
transference  of  the  line  of  gravity  to  the  active  leg  also  takes  part  in 
this  action  by  removing  the  fixed  point,  from  which  the  muscles  of  the 
passive  leg  act,  from  the  foot  to  the  pelvis. 

(e)  The  Act  of  Acquiring  the  Erect  Posture. — Now,  if  the  changes 
of  position  which  take  place  in  walking  are  due  to  the  predominance  of 
cerebro-spinal  over  cerebello-spinal  action,  this  is  no  less  true  with 
respect  to  the  successive  changes  of  posture  requisite  to  raise  the  body 
from  the  recumbent  to  the  erect  posture.  Suppose  a  man  is  lying  in 
the  prone  position,  and  then  gets  up  on  his  hands  and  knees.  When 
the  knees  are  raised  by  muscular  action,  so  that  the  body  is  supported 
by  the  tips  of  the  fingers  and  the  toes,  while  the  centre  of  gravity  falls 

6 


<S2  PHYSIOLOGICAL    INTRODUCTION. 

midway  between  the  anterior  and  posterior  extremities,  this  constitutes 
what  I  may  call  the  quadrupedal  position:  In  this  position  the  toes 
constitute  the  fixed  point  for  the  posterior  extremities,  and  the  muscular 
strain  rests  upon  the  flexors  of  the  phalanges,  their  contraction  being 
necessary  to  maintain  the  rigidity  of  the  plantar  arch.  The  extensors 
of  the  foot  on  the  leg  must  contract  to  prevent  flexion  of  the  leg  at  the 
ankle,  the  extensors  of  the  leg  on  the  thigh  must  contract  in  order  to 
prevent  the  thigh  being  flexed  on  the  leg,  and  the  extensors  of  the 
body  on  the  thigh  must  also  contract  in  order  to  prevent  the  former 
being  flexed  on  the  latter.  A  further  contraction  of  these  same  muscles 
drags  the  centre  of  gravity  of  the  body  upwards  and  backwards,  the 
Aveight  is  taken  off"  the  anterior  extremities,  and  the  body  assumes  the 
semibipedal  posture,  in  which  the  line  of  gravity  passes  between  the 
feet  in  the  line  which  joins  the  toes,  considerably  in  front  of  the  line 
which  joins  the  ankles,  behind  that  which  joins  the  knees,  and  in  front 
of  that  joining  the  hip-joints.  It  is  manifest  that  the  contractions  of 
the  muscles  of  the  sole,  those  of  the  calf,  front  of  the  thigh,  those  of 
the  gluteal  region  and  the  erectors  of  the  spine,  must  largely  predomi- 
nate over  their  antagonists  in  order  to  maintain  this  position,  and  that 
this  predominance  must  be  maintained  until  such  time  as  the  heel 
touches  the  ground,  when  the  line  of  gravity  passes  from  the  toes  to 
the  centre  of  the  plantar  arch,  and  behind  the  line  joining  the  centre 
of  the  two  hip-joints.  The  vertical  position  is  then  maintained  mainly 
by  means  of  the  bones  and  ligaments,  aided  only  by  a  slight  degree  of 
muscular  contraction.  Now,  the  bipedal  erect  posture  has  only  been 
attained  from  the  recumbent  position  by  passing  through  an  infinity  of 
intermediate  postures,  and  according  to  the  hypothesis  the  cerebello- 
spinal system  has  had  to  maintain  each  posture  attained  by  striking  a 
balance  between  the  tensions  of  the  extensors  and  flexors  of  the  body, 
the  latter  being  aided  by  gravity  ;  while  the  cerebro-spinal  system  con- 
tinually changes  each  attained  posture  by  overthroAving  this  balance  in 
favor  of  the  extensors.  In  passing  from  the  bipedal  erect  posture 
through  the  semibipedal  and  quadrupedal  to  the  recumbent  posture  a 
reverse  process  takes  place,  the  cerebro-spinal  system  at  each  new  posi- 
tion ac(|uired,  inhibits  the  action  of  the  cerebello-spinal  system  on  the 
extensors,  so  that  contraction  of  the  flexors  assisted  by  gravity  is 
allowed  gradually  to  predominate. 

But  if  this  hypothesis  of  the  joint,  although  opposite,  action  of  the 
cerebrum  and  cerebellum  acting  through  the  spinal  cord  be  true  at  all, 
it  must  be  accepted  in  its  fullest  extent.  If,  for  instance,  it  be  true 
that  the  passage  from  what  I  have  called  the  quadrupedal  to  the 
bipedal  posture  in  the  human  subject  is  due  in  the  individual  to  the 


I 


CEREBRO-SPINAL    AND   CER  EBELLO  -  SPIN  AL   SYSTEMS.      83 

predominance  of  cerebral  influx  to  the  extensors  over  their  antagonists, 
thL^  is  no  less  true  with  respect  to  the  race.  In  the  gradual  develop- 
ment of  man  from  the  lower  animals  the  same  forces  have  been  at  work. 
From  the  seniibipedal  position  assumed  hj  a  dog  attempting  to  stand 
on  its  hind  legs,  and  the  imperfect  bipedal  attitude  of  the  monkey  to 
the  perfect  bipedal  posture  of  man,  the  transition  must  have  been 
effected  l)y  the  gradual  j)redoininance  of  the  extensors  over  their  antago- 
nists through  cerebro-spinal  influence.  In  all  these  processes  it  will  be 
seen  that  the  flexors  of  the  body  are  aided  in  their  action  by  the  force 
of  gravitation,  while  the  extensors  have  to  overcome  this  force  bv  their 
action,  hence  the  latter  must  be  capable  of  much  more  powerful  con- 
traction than  tilt'  former,  and  are  consequently  more  liable  to  have 
more  j)Owerful  discharges  sent  to  them  both  from  the  cerebro-spinal 
and  cerebel]o-s])inal  systems. 

When,  therefore,  both  the  extensors  and  flexors  of  the  head,  trunk, 
and  lower  extremities  are  contracted  to  their  utmost  capacity,  the  action 
of  the  former  must  predominate  over  that  of  the  latter ;  so  that  the 
segments  of  the  lower  extremities  will  be  extended  upon  one  another, 
and  the  body  will  be  arched  with  tlie  concavity  directed  backwards,  as 
occurs  during  the  paroxysms  of  tetanus.  But  the  hand  being  mainly 
an  organ  of  })rehension,  the  principal  functions  of  the  anterior  limbs  of 
man  is  to  pull  objects  towards  the  trunk,  the  latter  being  the  fixed 
point  during  their  activity,  hence  the  flexors  of  the  upper  extremities 
must  be  more  strongly  developed  than  the  extensors.  And  when  the 
hands  become  fixed,  as  in  climbing,  the  most  powerful  contractions  are 
obtained  when  they  are  in  a  ])osition  to  drag  the  body  towards  the 
fixed  ])Osition,  and  not,  as  in  the  case  of  the  lower  extremities,  when 
the  body  is  thrust  upwards  and  away  from  it ;  hence,  when  the  muscles 
of  the  upper  extremities  are  contracted  to  their  utmost  capacity,  flexion 
will  predominate  over  extension. 

[f)  Fundamental  and  Accessory  Portions  of  the  Nervous  System. — 
Before  leaving  this  })orti()n  of  our  subject  I  should  like  to  establish  one 
more  distinction.  Structure  being  the  correlative  of  function,  the  mul- 
tiplicity and  complexity  of  the  movements  which  distinguish  man  from 
the  lower  animals  must  be  accompanied  by  a  corresponding  degree  in 
the  intricacy  ;ind  variety  of  the  structui'al  arrangements  of  his  nervous 
system.  The  main  movements  which  distinguish  man  from  the  lower 
animals  are  tjiose  concerned  in  attaining  and  maintaining  the  erect 
posture,  the  varied  movements  of  the  hands  as  organs  of  prehension, 
the  movements  of  voice  and  articulation  concerned  in  speech,  and  those 
which  are  active  in  the  production  of  facial  expression.  All  these 
movements  must,  therefore,  be  represented  in  the  human  nervous  system 


34  PHYSIOLOGICAL    IXTRODUCTIOX . 

by  structural  arrangements  superadded  to  those  Avliich  man  possesses  in 
common  with  the  highest  of  the  lower  animals.  Indeed,  all  the  cgm- 
plex  movements  first  mentioned  are  accjuired  considerably  after  the 
birth  of  the  human  infant,  and  we  may  conse(iuently  expect  that  the 
structural  arrangements  corresponding  to  them  eitlier  do  not  exist  at 
birth  or  exist  only  in  an  embryonic  condition. 

The  portions  of  the  nervous  system  which  man  possesses  in  common 
with  the  lower  animals,  and  which  are  well  developed  in  the  human 
embryo  at  nine  months,  I  shall  call  the  fundamental  part,  and  the 
portions  which  have  been  superadded  in  the  course  of  evolution,  which 
differentiate  the  nervous  system  of  man  from  that  of  the  highest  of  the 
lower  animals,  and  which  are  either  absent  in  the  human  eml)ryo,  or 
exist  only  in  an  embryonic  condition,  I  shall  call  the  accessory  part  of 
the  nervous  system. 

The  fundamental  portion  of  the  human  nervous  system  coordinates 
the  fundamental  functions  which  man  possesses  in  common  with  the 
lower  animals,  but  the  accessory  portions  can  only  l>e  said  to  regulate 
the  accessory  functions  in  a  peculiar  sense.  The  accessory  structure 
constitutes  indeed  a  new  complexity  of  mechanism  superadded  to  that 
already  existing,  a  complexity  rendered  necessary  for  the  regulation  of 
the  intricate  and  multiform  actions  Avhich  distinguisli  man  from  the 
lower  animals.  In  the  develo])ment  of  the  accessory  system,  small 
round  cells  and  non-medullated  fi])res  appear  at  a  comparatively  late 
period  in  the  development  of  the  embryo,  and  the  presence  of  these 
simple  elements  may  be  regarded  as  the  structural  counterpart  of  a 
new  modification  or  specialization  of  function.  Specialization  of  func- 
tion has  hitherto  been  connected  with  the  gradiuil  development  of 
medullated  from  non-medullated  fibres,  and  of  large  caudate  fi'om  small 
round  cells ;  but  now  it  appears  that  specialization  of  function  is  to  be 
connected  with  the  development  of  embryonic  cells  and  fibres.  There 
is,  however,  no  contradiction  between  the  two  statements.  The  em- 
bryonic cells  and  fibres  of  the  accessory  system  do  not  of  themselves 
indicate  any  specialization  of  function.  I'hese  cells  and  fibres  are, 
indeed,  mere  complications  of  an  already  existing  mechanism,  and  it  is 
this  alone  which  entitles  them  to  be  regarded  as  true  indicators  of  a 
newly  acquired  specialization  of  function ;  they  are,  in  short,  mere 
modifications  of  an  already  existing  structure  corresponding  to  newly 
acquired  modifications  of  previously  existing  muscular  adjustments. 
There  can  1)e  no  doubt  that  the  fundamental  and  accessory  portions  of 
the  nervous  svstem  will  be  so  min";led  together  that  it  will  be  almost 
impossible  to  separate  the  two,  but  whether  they  can  be  distinguished 
from  one  another  morphologically  or  not,  the  mental   distinction  is  a 


CKRl-:i?R()-SI'IXAI,  AXD  CE  R  EBELLO  -  SP  IN  AL  SYSTEMS.   85 

valuable  one,  and  it  -will  Ije  found  of  importance  to  remember  that  in 
man  the  cephalic  ganglia,  the  central  gray  tube,  the  conducting  paths, 
and  even  the  peripheral  nerves,  Jimst  contain  fundamental  and  accessory 
cells  and  fibres. 

A  comparison  of  the  brain  of  man  Avith  that  of  the  monkey  will 
afford  a  rough  test  by  which  we  may  distinguish  the  accessory  portions 
of  the  former  of  the  two.  Passing  over  such  obvious  considerations  as 
distinctions  of  size  and  weight,  the  first  important  difference  we  note  is 
the  great  relative  increase  in  the  size  of  the  frontal  lobe  in  the  brain  of 
man.  The  relative  increase  of  this  lobe  causes  the  posterior  lobes  to 
be  thrust  further  backwards  over  the  cerebellum,  the  fissure  of  Rolando 
to  slant  upwards  and  backwards  instead  of  being  vertical,  as  in  the 
brain  of  the  monkey,  and  the  posterior  limb  of  the  Sylvian  fissure  to 
become  longitudinal  instead  of  slanting  upwards,  as  in  the  Simian 
brain.  It  is  likely  that  the  large  relative  size  of  the  frontal  lobe  in 
num  is  connected  with  his  mental  superiority  over  the  monkey.  The 
next  difference  we  observe  is  the  depth  of  the  fissures  in  the  brain  of 
man  as  compared  with  that  of  the  monkey.  In  the  course  of  develop- 
ment the  summits  of  the  convolutions  are  first  formed,  and  they  alone 
are  directly  connected  with  the  incoming  and  outgoing  fibres  of  the 
cerebro-spinal  conducting  paths.  The  infolding  of  the  cortex,  which 
forms  a  sulcus,  is  a  later  result  of  development,  and,  as  the  superficial 
extent  of  the  cortex  becomes  greater  and  greater,  the  deeper  the  sulci 
become,  so  the  depth  of  the  sulci  may  be  taken  to  some  extent  as  a 
measure  of  the  development  of  the  brain.  The  next  point  we  note  is 
the  great  complexity  of  the  arrangement  of  the  convolutions  in  the 
brain  of  man  as  compared  with  that  of  the  monkey.  The  convolutions 
of  the  human  brain  are  divided  into  primary  or  fundamental  and 
st'condary  or  accessory.  The  fundamental  convolutions  in  man  are 
distributed  along  the  margins  of  the  great  longitudinal  fissure  and  other 
primary  fissures,  like  the  Sylvian  fissure  and  the  fissure  of  Rolando, 
and  their  disposition  corresponds  closely  with  the  arrangement  of  the 
convolutions  in  the  brain  of  the  monkey.  The  accessory  convolutions 
of  man,  which  are  rather  irregular  in  their  distribution,  may  be  re- 
garded as  structures  superadded  in  the  course  of  evolution.  These 
convolutions  are  connected  with  the  primary  convolutions  by  arcuate 
fibres,  and  are  not  directly  connected  with  the  ascending  and  radiating 
fibres  of  the  internal  capsule,  and  consequently  their  activity  is  likely 
to  be  correlated  with  mental  operations.  Another  remarkable  feature 
in  which  the  human  brain  diff"ers  from  the  brain  of  animals  is  the 
manner  in  which  the  Island  of  Reil  is  completely  surrounded  and 
hidden  out  of  view  by  deep  convolutions.     This  is  brought  about  by 


80 


PHYSIOLOGICAL    INTRODUCTION, 


the  large  development  of  the  posterior  extremity  of  the  inferior  frontal, 
of  the  Inferior  extremities  of  the  ascending  frontal  and  parietal  convo- 
lutions, and  of  the  supra-marginal,  angular,  and  temporo-sphenoidal 
gvri.  The  consequence  of  the  large  development  of  these  convolutions 
is  that  the  cortex  is  deeply  folded  over  the  Island  of  Reil,  this  fold 
forming  a  kind  of  hood,  which  has  been  named  the  operculum.  It  ap- 
pears to  me  that  the  cortex  of  the  Island  of  Reil,  starting  from  the 
gray  matter  of  the  anterior  perforated  space,  is  the  embryonic  part  of 
the  cortex  of  the  brain,  just  as  the  central  gray  column  is  the  embryonic 

Tig.  4;'!. 


Horizontal  Section  ok  the  Basal  Ganglia  and  Inteksal  C'apsvle  of  a  Nine  .Months'  Kmbrvo. 
II,  in,  Second  and  third  segments  of  the  nucleus  respectively  ;   NC,  Caudate  nucleus ;    TH,  Optic 
thalamus  ;  IN,  Island  of  Keil ;  ps,  Peduncular  sensory  tract  and  optic  radiations  of  Gratiolet ;  P,  Fnndii- 
mental,  P',  Mixed,  and^),  Accessory  portion  of  pyramidal  tract  ;  C,  Fibres  from  the  corpus  callosum  i?). 


portion  of  the  gray  matter  of  the  spinal  cord.  On  the  supposition  that 
the  portion  of  the  Island  of  Reil  which  lies  in  the  line  of  distribution 
of  the  Sylvian  artery  is  the  embryonic  portion  of  the  convolutions  of 
the  motor  area  of  the  cortex,  it  may  be  expected  that  the  earlier  formed 
portions  of  these  convolutions  will  be  thrust  upwards  towards  the  great 
longitudinal  fissure,  while  the  later  formed  pin-tions  will  approach  nearer 
and  nearer  to  the  root  of  the  artery.  According  to  this  supposition,, 
therefore,  the  fundamental  portions  of  the  convolutions  supplied  by  the 
Sylvian  artery  Avill  be  found  near  the  great  longitudinal  fissure,  and  the 


("KRKBKO-SPIN  AL    A  X  D    (' K  R  K  ]5ELL0  -  S  P  1  N  A  L    SYSTEMS.       87 

accessory  portion  low  down  near  the  root  of  the  artery,  the  hast  portion 
being  formed  by  the  o))erculum.  This  opinion  corresponds  closely  with 
the  topoii-raphical  distribution  of  the  motor  centres  as  determined  l)v 
experiment  and  i)atliological  observation.  The  movements  of  the  mus- 
cles of  the  trunk,  which  must  be  regarded  as  the  fundamental  move- 
ments, are  regulated  from  the  marginal  convolutions  of  the  longitudinal 

Fio.  4)). 


P/  — 


Tkansveksf,  Section   oi-    iHh  <  ui:-  Cerebri   on   a   level   with   the   anterior  pair   of   Corpora 

QUADRKiEMINA,     FROM     A    NINE    MONTHS'     EMBRYO.      (Modified    froill    KraUSE.) 

ff,  cnista  ;  P,  pyrnniidal  tract ;  p,  accessory  portion  of  tlie  pyramidal  tract ;  LN,  locus  niger  ;  BK,  reil 
nuclous  of  the  tegmentum  ;  L,  posterior  longitudinal  fasciculus ;  or  and  ar',  upward  continuation  of  the 
internal  and  external  portions  respectively  of  the  anterior  root-zone  of  the  spinal  cord  ;  iii,  third  nerve  ; 
in',  nucleus  of  the  third  nerve  ;  iv,  fourth  nerve  ;  iv',  nucleus  of  the  fourth  nerve  :  iv",  crossing  of  the 
fibres  of  the  fourth  nerve  to  opposite  sides;  rf/,  descending  root  of  the  trigeminus;  cc,  aqueduct  of 
Sylvius  ;  X,  crossing  of  the  fibres  of  the  superior  peduncles  of  the  cerebellum  ;  pf,  fasciculus  of  meduUated 
fibres  proceeding  from  the  fillet  tn  the  anterior  pair  of  corpora  i|uadrigemiiia. 

sulcus  ;  while  the  movements  of  the  lips  and  tongue,  and  those  of  the 
small  muscles  of  the  hand,  Avhich  are  the  chief  accessory  movements, 
are  regulated  from  the  operculum. 

In  endeavoring  to  discriminate  ])etween  the  fundamental  and  acces- 
sory portions  of  the  C(mducting  paths,  the  most  efficient  practical  test 


ss 


PHYSIOLOGICAL    INTRODUCTIOX 


is  to  regard  all  those  fibres  which  are  fully  medullated  at  birth  as  be- 
lonsing^to  the  fundamental  system ;  and  those  which  are  non-meduUated 
at  birth,  but  afterwards  acquire  this  sheath,  as  belonging  to  the  acces- 
sory system. 

In  following  the  course  of  the  pyramidal  tract  downwards  from  the 
cortex,  its  fibres  come  together  to  form  one  bundle  in  ihe  anterior  two- 
thii-ds'of  the  posterior  segment  of  the  internal  capsule.  When  the 
internal  capsule  is  examined  at  birth  the  pyramidal  tract  consists  of  a 

Fig.  47. 


Tr.vxsvkrsf.  Sectiiin  of  the  Pons  on  a  i.f.vel  with  the  Ahuucens  akd  Kai'iai.  Hoots,  ekom  a  sine 

months'  embryo.  (Jlotlified  from  Kuu. ) 
The  right  lialf  repi'esents  a  section  made  a  little  lower  thau  the  left  P,  jiyramidal  tract  ;  ji,  accessory 
jiortiou  of  the  pyramidal  tract;  JV  and  TV',  transverse  fibres  of  the  pons;  so,  superior  olivary  body;  nlc 
and^^c,  anterior  and  posterior  nuclei  of  the  lateral  column  respectively,  representing  the  nucleus  of  the 
facial  nerve;  rvii,  root  of  the  facial  nerve  ;  vi',  nucleus  of  the  sixth  nerve  ;  rvi,  root  of  the  sixth  nerve  ; 
at,  ascending  root  of  the  trigeminus.  B,  The  internal  division  of  the  peduncle  of  the  cerebellum  as  it 
passes  from  the  cerebellum  ;  L,  posterior  longitudinal  fasciculus  ;  ar  anil  ar",  the  upward  continuation  of 
the  internal  and  external  divisions  of  the  anterior  root-zone  of  the  spinal  cord  ;  I,  fasciculus  teres. 

posterior  portion  (Fig.  47,  P)  in  which  all  the  fibres  are  medullated,  a 
middle  portion  (Fig.  45,  P')  in  which  medullated  and  non-medulla  ted 
fibres  are  mixed,  and  an  anterior  portion  (Fig.  45,  p)  in  which  all  the 
fibres  are  non-medullated.  In  the  crusta  the  medullated  fibres  lie  in 
the  outer  portion  of  the  middle  third  (Fig.  4(^  P),  the  mixed  fibres  in 
the  inner  portion  of  the  middle  third  (Fig.  4(!,  P'),  and  the  non-medul- 
lated fibres  in  the  inner  third  (Fig.  4(5,  p).     In  the  pons  the  medullated 


C  E  K  K  15  K  O  -  S  P  1  X  A  L    A  N  I)   C  K  E  E  B  E  L  L  O  -  S  P  1  X  A  L    SYS  T  E  :^I  S  .       89 

Hbres  lie  in  the  anterior  and  external  longitudinal  bundles  (Fig.  47,  P), 
and  the  non-niedullated  lie  in  the  anterior  and  internal  bundles  (Fif, 
47,  p),  while  the  bundles  of  mixed  fibres  lie  between  these.  In  the 
anterior  pyramid  of  the  medulla  the  medullated  fibres  occupy  the  pos- 
terior and  external  parts  of  the  pyramid  (Fig.  28,  P),  and  the  non- 
medullated  the  anterior  and  inner  side  (Fig.  28,  j))^  while  the  area  of 
mixed  fibres  lies  between  them.  It  is  probable  that  the  fibres  of  the 
medullated  area  form  the  conducting  paths  of  the  moA'^ements  of  the 
muscles  of  the  trunk  and  of  those  of  the  lower  extremities,  the  fibres 
of  the  mixe<l  area  tlie  conducting  paths  of  the  movements  of  the  hand, 
and  the  fibres  of  the  non-medullated  area  the  conducting  paths  of  the 
movements  of  articulation  and  facial  expression,  movements  which  are 
not  orL'anized  until  some  time  after  birth. 


CHAP  TEE   III. 

GENERAL  MORBID  ANATOMY  AND  PHYSIOLOdY  OF  THE 
NERVOUS  SYSTEM. 

I.  GENEKAL  MOKBID  ANATOMY. 

Disease  of  the  nervous  system  is  caused  (1)  by  defects  in  its  devel- 
opment or  evolution;  or  (2)  by  a  reversal  of  the  process  of  evolution,  or, 
in  other  words,  by  dissolution. 

1.  Defects  of  Dkvei-op.mhnt. 

a.  Congenital  Defects  of  Nerves. 

When  portions  of  the  body  are  incompletely  formed,  the  ner\es  are 
defective  or  absent.  When,  for  example,  the  nose  is  arrested  in  its 
development,  and  when  no  eyes  have  been  formed,  not  only  are  tlic 
optic  nerves  absent,  but  the  third,  fourth,  and  sixth  pairs  are  also  deti- 
cient.  In  a  Cyclops,  in  which  the  face  was  almost  entirely  wanting,  no 
facial  nerve  could  be  found,  and  when  the  ton<rue  is  wanting  the  lingual 
brandies  of  the  fifth  and  the  liyj)oglossal  nerves  are  absent.  In 
monsters  in  which  one  or  more  of  the  extremities  are  imperfect,  there  is 
a  corresponding  deficiency  in  the  nei'ves  of  that  limb  or  limbs. 

h.   Congenital  Defects  of  the  Spinal  Cord. 

(1)  Amyelia,  or  absence  of  the  spinal  cord.  Only  met  with  when 
the  brain  is  also  absent. 

(2)  Atelomyelia,  or  imperfect  development  of  the  spinal  cord.  The 
upper  end  of  the  cord  is  lacking  or  imperfectly  develoj)ed,  the  brain 
being  also  absent  {anencephalia),  or  the  head  defective  (acephalia).  The 
medulla  oblongata  is  absent  or  exists  only  in  a  rudimentary  form. 

(3)  Diastematomyelia  is  a  condition  in  which  the  two  lateral  halves 
of  the  cord  either  do  not  unite,  or  unite  only  throughout  a  portion  of 
their  extent.     This  malformation  occurs  with  anencephalia. 

(4)  Diplomyelia,  or  duplication  of  the  spinal  cord,  appears  in  the 
various  foi-ms  of  double  monsters. 


DEFECTS    OF    1)  E  VELO  P  M  EN 'J' .  <U 

(5)  Aiioiiialies  in  the  leiic/th  and  thickness  oi'  the  cord  are  sometimes 
ohscrved  the  organ  being  sometimes  thick  and  voluminous,  and  at' 
other  times  thin  and  small.  It  descends  at  times  to  the  third  lumbar 
\crtcbra.  and  ends  at  other  times  opposite  the  eleventh  or  twelfth 
dorsal.  A  small  si/e  of  the  spinal  cord  has  been  met  Avith  in  hered- 
itarv  ataxia. 

(('))  Asymmetry  of  the  (jray  substance  has  been  oljserved  in  cases  of 
i  iseudo-hypertrophic  paralysis,  and  more  especially  in  cases  of  con - 
Lienital  absence  of  one  or  more  of  the  extremities. 

(7)  The  pyramidal  tracts  are  absent  in  anencephalous  monsters, 
and  imperfectly  developed  in  some  cases  of  congenital  parencephalus. 
Each  anterior  ])yramid  of  the  medulla  may  also  send  the  mass  of  its 
libi'es  into  the  spinal  cord,  either  entirely  crossed  or  only  partially 
crossed,  or  down  the  anterior  columns  almost  entirely  uncrossed. 

(8)  Hydromyelus  congenitus,  or  hydrorrhachis  interna,  is  a  condition 
in  which  thei-e  is  a  congenital  enlargement  of  the  central  canal  of  the 
lord,  which  is  converted,  in  the  slighter  degrees  of  the  aftection,  into  a 
i-avitv  vai'vino-  from  the  size  of  an  ordinarv  knittincr-needle  to  that  of 
a  crow's  (piill.  The  dilated  canal  may  extend  the  whole  length  of  the 
i-ord,  be  restricted  to  certain  portions,  assume  a  moiiiliform  appearance, 

>  >r  present  the  appearance  of  a  double  canal  by  the  growth  of  adhesions 
lietween  the  anterior  and  posterior  walls.  In  the  higher  grades  of  con- 
genital hydromyelus  the  spinal  cord  either  disappears  entirely,  or  be- 
comes split  into  two  halves  for  a  greater  or  less  distance,  while  the 
cavity  of  the  central  canal  communicates  freely  with  the  cavity  of  the 
-])inal  arachnoid:  the  hydrorrhachis  interna  is  then  merged  into 
liydrorrachis  externa,  as  not  infrequently  happens  in  spina  bifida. 

(9)  Spina  bifida  consists  of  an  abnormal  accumulation  of  fluid  within 
rhe  cavity  of  the  sj)inal  arachnoid,  associated  with   a  greater   oi'    less 

lefonnity  of  the  s])inal  canal. 

c.   Gonyenital  Malformations  of  the  Skull  and  Brain. 

(1)  Anencephalia. — The  upj)er  portion  of  the  skull  and  Ijrain  is 
entirely  absent,  and  ip  occasionally  associated  with  amyelia. 

(2)  Heniicrania. — The  anterior  portion  of  the  skull  is  absent,  and 
the  brain  deficient. 

(o)  Heniicephalia. — The  lateral  half  of  the  liraiii  and  skull  is  de- 
ficient. 

(4)  Notmccphalus. — The  upper  part  of  the  skull  is  deficient,  and 
the  vertebral  column  is  not  entirely  closed  in,  the  brain  develoi)ing  in 
the  vertebral  canal  instead  of  in  the  skull. 


92  MORBID    ANATOMY    OF    THE    NERVOUS    SYSTEM. 

(;'))  ffydrencephalocele.— The  bones  of  the  skull  are  deficient,  an 
opening  being  left  through  which  a  soft  fluctuating  tumor  projects. 
The  walls  of  the  tumor  consist  of  the  soft  coverings  of  the  skull  and 
the  distended  membranes  of  the  brain.  The  tumor  c(mimunicates 
with  the  general  ventricular  cavity  of  the  brain,  and  can  generally  l)e 
emptied  on  steady  pressure. 

(<!)  Uncephalocde. — The  bones  of  the  skull  are  deficient,  and  through 
the  oi)ening  thus  caused  a  portion  of  the  brain  projects,  forming  a 
broad,  flat,  solid  tumor.  The  tumor  frequently  occupies  the  fu-ehead, 
orbit,  or  side  of  the  nose. 

(7)  Parencephalus. — A  portion  of  the  hemisphere  is  deficient,  but, 
as  it  is  not  always  caused  by  a  congenital  arrest  of  development,  it  will 
be  subsequently  described. 

(8)  Microcephalus  is  a  condition  in  which  the  brain  as  a  whole,  and 
probably  the  nervous  system  generally,  is  arrested  in  its  development. 
It  occurs  in  idiots,  and  the  brain  is  not  only  small  in  size,  but  its  con- 
volutions also  retain  the  simplicity  of  arrangement  which  characterizes 
the  Simian  brain. 

(9)  Neuropathic  constitution  is  a  condition  in  which  the  nervous 
inheritance  of  the  subject  is  shown  to  be  defective  b}"  a  functional 
incapacity  to  respond  adequately  to  the  ordinary  conditions  of  life,  but 
without  this  defect  being  apjwrent  to  our  means  of  investigation  in  the 
structure  of  the  nervous  system.  The  predisposition  to  a  particular 
disease  may  be  sjyecial  and  direct,  or  general  and  indirect.  Migraine, 
for  example,  may  be  transmitted  directly  from  a  mother  to  her  daughtei", 
and  the  attacks  of  headache  generally  appear  in  both  al)Out  puberty. 
In  such  a  case  the  transmission  is  direct  from  mother  to  daughter,  and 
the  transmitted  disease  is  limited  to  a  particular  aflFection.  But  the 
inheritance  in  this  case  is  also  immediate  as  well  as  direct  and  special, 
inasmuch  as  the  disease  is  directly  transmitted  from  parent  to  child. 
But,  in  a  large  number  of  diseases,  the  inheritance  is  remote^  the 
transmitted  affection  being  derived  not  immediately  from  the  parent, 
but  from  a  grandparent,  or  a  still  more  remote  ancestor.  The  ])he- 
nomena  of  atavism  or  reversion,  as  the  remote  inheritance  is  called, 
are,  indeed,  very  conspicuous  in  the  transmission  of  a  large  nundjcr  of 
nervous  diseases. 

In  other  cases  a  vulnerable  nervous  system,  named  a  neurotic  or 
neuropathic  disposition,  is  transmitted,  which  favors  tlie  appearance  of 
nervous  disease.  In  such  cases  the  tendency  to  any  particular  disease 
is  indirect;  and  it  is  also  general,  inasmuch  as  one  member  of  a  family 
may  suffer  from  neuralgia,  another  from  chorea,  paralysis,  hysteria, 
epilepsy,  or  insanity,  while  others  mav  manifest  a  tendencv  to  uncon- 


DISSOLUTION    OF    THE    NEKYOUS    SYSTEM.  03 

trollablo  alcoholic  excesses.  At  other  times  the  predisposition  to  ner- 
vous disease  is  still  more  indirect.  One  man  dies  of  disease  of  the 
brain,  as  his  father  did  before  him,  at  a  particular  age,  but  it  is  because 
both  have  inherited  gout,  which  has  induced  early  arterial  degeneration, 
whieh  in  its  turn  has  ended  in  rupture  of  a  bloodvessel  in  the  brain. 
In  another  family  several  children  die  about  the  same  age  after  convul- 
sions and  coma,  but  it  is  because  they  have  inherited  a  strong  tendency 
to  tubercular  disease,  and  not  from  inherent  weakness  of  the  nervous 
system.  The  inherited  tendency  to  certain  nervous  diseases  is  strongly 
influenced  by  age,  sex,  and  race ;  but  this  point  need  not  detain  us  at 
in-esent. 

2.  Dissolution  of  the  Nervous  System. 

The  law  of  dissolution  is  the  converse  of  evolution,  and  may  be 
enunciated  as  a  progressive  disintegration  both  of  structure  and  func- 
tion, in  which  there  is  a  passage  from  the  complex  to  the  simple,  from 
the  multiform  to  the  uniform,  and  from  the  special  to  the  general. 
Before  discussing  further  the  application  of  the  law  of  dissolution  to 
the  phenomena  of  the  diseases  of  the  nervous  system,  it  will  be  useful 
to  classify  the  lesions  to  which  the  nervous  system  is  liable — the  term 
lesion  being  used  hei'e  as  a  generic  expression  to  indicate  any  morbid 
alteration  of  tissue,  whether  this  alteration  be  or  be  not  attended  by 
such  structural  chan^-es  as  can  be  recoo-nized  after  death  by  our  means 
of  research. 

Classification  of  Lesions  of  the  Nervous  System. 

Lesions  of  the  nervous  system  may  be  classified  (1)  according  to  their 
nature ;  (2)  according  to  their  form  :  (3)  according  to  the  functional 
disturbances  they  produce. 

(1)  Classification  According  to  the  Nature  op  the  Lesion. 

(1)  lyiflatnmation. — Every  part  of  the  nervous  system  is  subject  to 
inflammation,  which,  like  inflammation  of  other  tissues,  may  be  acute, 
subacute,  or  chronic,  -with  respect  to  its  course  and  development.  When 
the  affection  is  acute  it  generally  ends  in  complete  disintegration  of  the 
affected  tissue,  which,  on  being  mixed  up  with  fluid  and  morphological 
elements  eff"used  from  the  bloodvessels,  ])resents  a  i)ulpy  mass  technically 
called  softening.  When  the  inflammatory  process  is  clironic  the  tissue 
undergoes  degeneration ;  but,  inasmuch  as  degeneraticm  may  occur 
independently  of  inflammation,  ])oth  kinds  may  be  included  in  one 
group. 


il4  MORBID    ANATOMY    OF    THE    NERVOUS    SYSTEM. 

(i^)  Degenerations. — Degenerations  of  nervous  tissues  are  of  various 
kinds  ;  ))ut  inasmuch  as  in  all  of  them  the  nervous  tissue,  instead  of 
undero-oino-  softenino-  as  in  acute  inflammation,  becomes  somewhat  denser 
than  usual,  they  are  called  scleroses.  From  the  color  of  the  altered 
tissue,  it  is  sometimes  called  gi-ay  dcfiencration.  Both  inflammations 
and  degenerations  include  afiectious  which  have  begun  in  the  connective 
tissues  or  neuroglia,  the  vessels  and  their  adventitite,  or  the  blood  itself, 
as  well  as  those  which  are  primarily  of  parenchymatous  origin. 

(3)  Vaseular  Lesion.^. — Besides  the  vascular  lesions  which  accom- 
pany all  inflammatory  and  degenerative  processes,  other  very  important 
diseases  in  connection  with  the  vessels  must  be  mentioned. 

{a)  Hypcrcemia  and  Ancemia. — The  vessels  are  at  times  actively 
dilated  so  that  an  undue  quantity  of  blood  is  sent  to  portions  of  the 
nervous  system,  while  they  are  at  other  times  contracted  so  that  the 
normal  quantity  is  diminished.  The  hyperaemia  may  at  times  be  active 
and  due  to  high  arterial  tension  and  active  dilatation  of  the  ai'terioles. 
while  at  other  times  it  is  passive,  and  is  then  caused  by  some  obsti-uc- 
tion  of  the  blood  along  the  large  veins  of  the  body.  The  ani^mia  to 
wliich  the  nervous  system  is  subject  does  not  differ  from  the  anaemia  of 
other  organs,  and  may,  therefore,  be  due  to  an  alteration  of  the  quality 
as  Avell  as  the  ([uantity  of  the  blood. 

[h)  Hemorrhage. — Ru})ture  of  vessels  with  consequent  hemorriiage 
is  a  very  common  cause  of  disease  of  the  central  nervous  organs,  and 
especially  of  the  cerebrum.  The  rupture  may  at  times  be  due  to  acci- 
dental injury,  but  more  freiiuently  it  occurs  in  the  degenerative  period 
of  life,  and  is  then  caused  by  various  degenerations  of  the  coats  of  the 
vessels,  such  as  atheroma  and  the  fibrosis  which  accompanies  Bright"> 
<lisease. 

(c)  Emholism  and  Thronhosis. — The  morbid  processes  of  embolism 
and  thrombosis,  when  they  occur  in  the  nervous  system,  are  essentially 
the  same  as  in  any  of  the  other  organs  of  the  body.  The  sudden  arrest 
of  the  circulation,  caused  by  obliteration  of  an  artery,  causes  intense 
anaemia  and  loss  of  function  of  the  part  to  which  its  branches  are  dis- 
tributed. The  centre  of  the  ischaemic  region  usuallv  underjjoes  necro- 
biosis,  and  its  substance  becomes  altered  into  a  soft  pulpy  mass  closely 
resembling  inflammatory  softening. 

(4)  Toxic  Lesions. — Various  chemical  agents  circulating  in  the  blood 
induce  morbid  alterations  of  the  nervous  tissues. 

(5)  Traumatic  Injuries. — Wounds,  contusions,  and  other  traumatic 
influences  cause  so  many  alterations  of  nervous  tissues  that  their  results 
deserve  to  be  mentioned  amongst  the  morbid  lesions  of  the  nervous 
system. 


DISSOLUTION    OF    THE    NERVOUS    SYSTEM.  95 

(6)  Compression  of  Nervous  Tismes. — The  ner\()us  tissues  are  fre- 
(|uently  subjected  to  sudden  or  gradual  compression  from  various  causes. 
One  of  the  most  frequent  causes  of  compression  is  the  gradual  encroach- 
ment on  the  tissues  of  new  formations,  no  matter  whether  the  growth 
l)e  outside  the  nervous  tissues  or  extra-neural,  or  in  the  substance  of  the 
tissues  or  intra-7ieural.  Other  causes  of  compression  are  fractures  of 
the  cranium,  dislocations,  fractures  and  curvatures  of  the  vertebrae,  the 
formation  and  subsequent  enlargement  of  abscesses  and  aneurisms,  and 
the  growth  of  cjsticerci  and  other  jiarasites.  Inflammatory  effusions 
and  thickenings  of  the  membranes  of  the  brain  or  cord,  or  of  the  sheaths 
of  nerves,  also  injure  the  nerve  tissues  by  compression  as  well  as  by 
extension  of  the  morbid  process  to  the  nervous  tissues  themselves. 

(2)  Classification  According  to  the  Form  of  the  Lesion. 

(1)  Circiimserihed  or  Focal  and  Diffused  Lesions — Systematic  Dis- 
eases.— When  a  lesion  is  circumscribed  within  definite  limits  it  is  called 
•A.  focal  lesion,  and  when  it  extends  over  an  iiidefinite  area  with  irregular 
limits  it  is  called  a  diffused  lesion.  "When  the  lesion  is  limited  to  a 
portion  of  the  nervous  s^^'stem  which  possesses  a  distinct  functional  unity, 
it  is  called  a  system-disease  or  a  systematic  lesion;  and  when  several 
physiological  tracts  are  implicated,  it  is  called  a  mixed  disease,  or  indis- 
criniinate  lesion.  A  lesion  limited  to  the  pyramidal  tract  in  the  sj)inal 
cord  is  a  good  example  of  a  systematic  lesion,  and  a  transverse  myelitis 
of  an  indiscriminate  lesion. 

(2)  3folecular,  Molar,  and  Histological  Lesions. — In  order  to  study 
these  diseases  under  the  simjdest  conditions,  let  us  suppose  that  the 
sciatic  nerve  of  a  frog  is  isolated,  with  the  gastrocnemius  muscle  at- 
tached. On  being  stimulated  by  a  strong  faradic  current,  the  muscle 
immediately  contracts ;  but  a  second  shock  through  the  nerve  is  poAver- 
less  to  induce  a  contraction — the  nerve  is  paralyzed.  During  the  pas- 
sage of  the  nerve  from  almost  perfect  health  to  complete,  though  tem- 
porary, paralysis,  the  change  which  it  has  undergone  is  such  as  cannot 
be  detected  by  the  most  refined  chemistry,  or  by  the  aid  of  the  highest 
powers  of  the  microscope.  In  such  case  we  assume  that  the  molecules 
of  the  axis-cylinder  have  come  to  a  condition  of  stable  equilibrium  ; 
hence  the  cause  of  the  loss  of  function  may  be  described  as  a  molecular 
lesion.  It  need  scarcely  be  added  that  a  molecular  lesion  may  also  give 
rise  to  excess,  as  well  as  diminution,  of  functional  activity.  The  lesion 
which  I  have  called  7nolecular  has  also  been  termed  functional,  from 
the  fact  that  the  part  affected,  while  giving  rise  to  definite  functional 
disturbances,  does  not  present  any  apparent  structural  changes. 

But  if  a  portion  of  the  sciatic  nerve  be  crushed  or  cut,  the  conductivity 


96  MORBID    ANATOMY    OF    THE    NERVOUS    SYSTEM. 

of  the  nerve  is  destroyed  at  tlie  point  of  injury,  and  a  faradic  current 
applied  to  the  nerve  on  the  central  side  of  the  injury  Avill  not  cause  the 
muscle  to  contract.  The  loss  of  function  in  this  case  is  caused  by  a 
lesion,  which  can  l)e  recognized  by  the  naked  eye ;  hence  it  may  be 
called  a  molar  lesion.  Dr.  Hughlings  Jackson  has  proi)OSed  to  call  the 
molar  lesion  1)y  the  name  of  "  coarse  disease,"  and  the  molecular  lesion 
by  the  name  of  "fine  disease"— names  which,  at  least,  possess  the  merit 
of  explaining  themselves.  Between  the  fine  or  the  molecular  lesion  on 
the  one  hand,  and  the  coarse  or  molar  lesion  on  the  other,  another 
variety  may  l)e  interposed.  When  the  morphological  elements  of  tlie 
nervous  tissues  themselves,  or  of  the  tissues  by  which  the  nervous 
elements  are  surrounded,  undergo  alterations  wliich  can  l)e  recognized 
by  the  aid  of  the  microscope,  the  morl)id  change  of  structure  may  l)e 
called  a  Jnstological  lesion. 

(3)  Classification  according  to  the  Alterations  of  Function  Produced 

BY  THE  Lesion. 

(1)  Irritative  and  Depressive  Lesions. — Wlien  the  morI>id  alteration 
is  attended  during  life  with  excess  of  functional  activity,  it  is  inferred 
that  the  lesion  is  one  of  an  irritative  character;  or,  in  other  words,  it  is 
inferred  that  the  irritability  of  the  cells  and  fibres  of  the  part  affected 
is  increased.  The  opposite  condition,  in  wliicli  the  irritalulity  is  dimin- 
ished or  abolished,  deserves  a  special  name  and  may  be  called  a  de- 
pressive lesion. 

(2)  I)is<-har(iing  and  I>estroying  Lesions. — Tlie  morbid  alterations 
which  are  attended  by  paroxysmal  and  excessive  liberations  of  energy 
have  been  called  by  Dr.  Hughlings  Jackson  discharging  lesions.  AVi- 
have  seen  that  the  nerve  cells  are  the  main  generators  and  accumulatoi-s 
of  energy,  hence  these  lesions  always  im])licate  the  gray  substance, 
although  it  is  not  always  easy  to  draw  a  shar]»  line  of  distinction  between 
discharges  of  eneruv  from  f^rav  substiince  and  those  which  result  from 
irritation  of  nerve  fibres.  When  the  affection  is  accompanied  by  a 
distinct  destruction  of  nerve  tissue,  such  as  occurs  in  hemorrhage  into 
the  substance  of  the  brain,  Dr.  Hughlings  Jackson  has  named  it  a 
destroying  lesion. 


(1)  Dissolution  of  JVerve  Cells  and  Fibres. 

a.  Morbid  Changes  of  the  Ganglion  Cells. 

(1)  Hypertrophy. — In  acute  inflannnation  the  ganglion  cells  become 
swollen,  their  contents  are  cloudy  and  granular,  and  often  pigmented, 
and  their  processes  also  participate  in  the  same  changes  (Fig.  48,  2). 


DISSOLUTIOX    OF    THE    XERVOUS    SYSTEM. 


97 


(-2)  Shrinking. — In  the  acute  diseases  of  the  f,nay  suhstance  of  the 
cord  the  fluid  contents  of  some  of  the  ganglion  cells  appear  to  escape, 
I  he  cell-wall  shrinks  around  the  nucleus  and  a  small  quantity  of  yel- 
l(.Av  pigment,  and  the  cell  is  contracted  into  a  shrivelled  mass,  which 
only  presents  slight  traces  of  its  former  structure   (Fig.  48,  4).     At  a 

Fig  48. 


Ganglion  Cells  of  the  Anterior  Gray  Horns  of  the  Spixal  Cord.    (Young.) 

1,  Healthy  caudate  cell;  2,  Hypertrophied  cell;  3,  Yellow  degeneration  (the  yellow  color  cannot  be 
represented  here) ;  4,  Shrivelled  cell ;  5,  Chronic  atrophy,  a  group  of  cells  from  a  case  of  pseudo-hyper- 
trophic  paralysis,  C,  Pigmentary  atrophy;  7,  Vacuolation,  from  a  case  of  canine  chorea  (Gowers)  ; 
8,  (  iironic  atrophy,  I'lum  a  case  of  progressive  muscular  atrophy — "yellow  atrophy." 


subsequent  period  these  cells  lose  their  processes  and  become  converted 
into  small  angular  masses,  in  which  even  a  nucleus  can  scarcely  be 
detected. 

(3)  Multiplication  of  the  Nucleus  and  Nucleolus. — Tlie  nucleus 
and  nucleolus  may  at  times  be  observed  either  to  have  divided  into  two, 
or  to  exhibit  an  hour-glass  contraction  indicating  that  the  process  of 
division  has  commenced. 


98 


MORBID  ANATOMY  OF  THE  NERVOUS  SYSTEM. 
Fig.  49. 


Alterations  in  Nerve  Fibres  after  Section.  (After  Ranvier.) 
1  and  2.  Two  nerve  fibres  from  the  peripheral  segment  of  the  sciatic  nerve  of  a  hare  fifty  hours  after 
section,  examined  after  maceration  for  twenty-four  hours  in  a  solution  of  perosmic  acid;  (n)  nucleus  of 
interannular  segment,  swollen  and  detached  from  the  sheath  of  Schwann  ;  (p)  mass  of  protoplasm,  in 
which  fat  granules  and  drops  of  myeliue  {g  and  my)  may  be  observed.  The  medullary  sheath  is  com- 
pletely interrupted  at  the  level  of  the  nucleus,  while  at  a  it  has  undergone  strangulation. 


DISSOLUTION    OF    THE    NERVOUS    SYSTEM.  1)9 

;i.  Ap|iearance  presented  by  the  peripheral  fibres  four  days  after  section  of  the  sciatic  nerve  of  a 
hare,  originally  hardened  in  a  solution  of  bichromate  of  ammonia  and  stained  by  picrocarmine  ;  (cy)  frag- 
ments of  the  axis-cylinder  retracted,  somewhat  tortuous  and  embedded  in  a  mass  of  myeline  (my) ; 
tp)  protoplasm  swollen  and  granular. 

4.  Fibre  same  as  3,  but  originally  colored  by  picrocarmine  after  maceration  in  perosraic  acid ;  (h)  nucleus 
compressing  and  partially  interrupting  the  medullary  sheath  and  the  axis-cylinder  ;  p,  protoplasm. 

5  and  6.  Fibres  from  the  peripheric  portion  of  the  sciatic  nerve  of  a  pigeon  three  days  after  section 
(same  method  of  preparation  as  4).  5.  Jledian  portion  of  an  interannular  segment  presenting  a  single 
swollen  nucleus  (»)  surrounded  by  a  mass  of  protoplasm  (p).  6.  Presents  four  nuclei  (n"  n"  n"  n")  in  a 
single  interannular  segment.  The  protoplasm  {p)  which  surrounds  them  is  not  segmented,  but  contains 
masses  of  myeline  in  its  interior. 

7  Fibres  from  the  central  end  of  the  sciatic  neive  of  a  hare  ninety  days  after  section  (same  method  of 
preparation  as  4).  Dark  upper  portion  represents  primitive  nerve  fibre  surrounded  by  the  sheath  of 
Schwann  (s),  and  terminating  by  a  knobby  enlargement  of  its  medullary  sheath  (h).  From  the  extremity 
of  this  termination  a  second  tube  (l')  issues,  which  divides  and  subdivides  until  it  forms  a  bundle  of  verj- 
fine  medullary  fibres  (F),  surrounded  by  a  secondary  sheath  (s*)  emanating  from  the  sheath  of  Schwann; 
m,  drops  of  myeline  derived  from  the  old  nerve  fibre. 

8.  .\  large  nerve  fibre  of  the  central  extremity  of  the  pneumogastric  nerve  of  a  hare  seventy-two  days 
after  section — maceration  in  perosmic  acid.  The  medullary  sheath  (t)  terminates  by  a  knobby  extremity 
(6),  and  from  this  extremity  secondary  medullated  nerve  tubes  (<'<";  issue,  as  well  as  fibres  without 
myeline  ;  (s)  the  sheath  of  Schwann  of  the  primary  fibre  forming  secondary  nerve  sheath  (s')  for  the 
nerve  fibres  which  issue  from  it. 

9.  A  nerve  tube  of  the  peripheric  segment  of  the  pneumogastric  of  a  hare  six  days  after  section.  The 
portions  a  a,  which  are  neither  occupied  by  drops  of  myeline  nor  by  nuclei,  are  collapsed,  and  the  tube  is 
contracted  at  this  level,  n  n,  nuclei  of  the  interannular  segment,  having  undergone  proliferation ; 
m  m,  drops  of  myeline. 

(4)  Vacuolation. — Two  or  tliree  large  .spherical  air-space.s  named 
vacuoles^  may  sometimes  be  observed  in  ganglion  cells  which  have 
undergone  a  granular  degeneration  (Fig.  48,  7). 

("))  Colloid  Dejjeneration. — The  hjpertrophied  cells  of  the  early 
stage  of  inflammation  may  subsequently  undergo  colloid  degeneration. 
Their  processes  become  transparent,  glistening,  and  brittle,  while  a 
large  portion  of  them  are  broken  off  so  that  the  cells  assume  a  rounded 
form.  The  cell-wall  has  a  glassy  appearance,  and  assumes  brilliant 
tints  when  stained  by  various  aniline  dyes.  The  colloid  appearance 
may  be  the  result  of  post-mortem  changes,  and  consequently  con- 
siderable cauti(m  must  be  exercised  in  accepting  them  as  evidence  of 
disease. 

(6)  Pigmentary  Dcijcneration. — The  best  examples  of  pigmentary 
degeneration  are  seen  in  the  chronic  diseases  of  the  spinal  cord.  The 
cell-wall  becomes  contracted  around  a  mass  of  dark  granular  pigment, 
the  nucleus  and  nucleolus  are  indistinct  or  obliterated,  the  processes  are 
atrophied,  and  many  of  them  have  disappeared  (Fig.  48,  6). 

(7)  Atrophy. — In  chronic  diseases  the  cell-wall  becomes  dense  and 
contracted,  the  processes  are  broken  oif,  and  the  remnant  of  the  cell  is 
contracted  into  a  small  angular  mass,  without  recognizable  nucleus  or 
nucleolus,  and  finally  all  traces  of  the  cell  may  be  lost  (Fig.  48,  5  and  8). 

(8)  Calcareous  Degeneration. — This  form  of  degeneration  is  ob- 
served on  rare  occasions. 


100        MORBID    ANATOMY    OF    THE    XERVOUS    SYSTEM. 

Although  tlic  iUustnitions  of  the  morbid  alterations  of  ganglion  cells 
have  been^taken  from  disease  of  the  caudate  cells  of  the  anterior  gray 
horns  of  the  spinal  cord,  yet  essentially  the  same  changes  are  met  Avith 
in  the  ganglion  cells  of  other  parts  of  the  nervous  system,  and  notably 
in  thos'e  of  the  cortex  of  the  brain.  It  is  scarcely  necessary  to  point 
out  how  these  various  alterations  conform  to  the  law  of  dissolution. 
These  alterations,  taken  as  a  whole,  are  a  passage  from  the  complexity 
and  nudtiformity  of  the  caudate  cells  with  their  numerous  processes  and 
well-defined  connections  to  the  simplicity  and  uniformity  of  the  round 
cell  without  processes  or  definite  connections. 

b.  Morbid  Changes  of  Nerve  Fibres. 

(1)  Wallerian  Degeneration. — The  most  notable  morbid  alterations 
of  nerve  fibres  are  best  studied  in  the  peripheral  ends  of  divided  nerves. 
"When  the  ])eripheral  portion  of  a  divided  nerve  is  examined  two  days 
after  section,  the  medulla  of  the  divided  fibres  is  found  to  be  coagulated, 
opaque,  granular,  and  broken  up  into  cylindrical  masses  (Fig.  49, 1,  2). 
The  imcleus  (?()  of  the  interannular  segment  has  l)ec()me  increased  in 
size,  and  contains  a  large  and  well-marked  nucleolus.  The  protoplasm 
which  surrounds  the  nucleus  becomes  so  al)undant  and  well  develo])ed  at 
the  level  of  the  nucleus,  that  it  fills  the  calibre  of  the  nerve  tube,  and 
completely  interrupts  the  medullary  sheath.  The  protoplasm  at  this  level, 
and  at  other  points  where  it  also  accumulates,  becomes  filled  with  fine 
fat  "Tanules  into  which  the  myehne  has  been  converted,  and  a  similar 
granular  debris  may  be  observed  outside  the  sheath  of  Schwann,  and 
in  the  substance  of  the  cells  of  the  endoneuriuni.  Duririij;  the  next 
two  or  three  days  the  segmentation  of  the  medullary  sheath  proceeds, 
and  the  cylindrical  masses  become  broken  up  into  globular  masses 
(Fig.  49,  5,  6),  which,  at  the  end  of  the  first  week  after  section,  are 
converted  into  drops  of  variable  size,  amongst  Avhich  a  progressively 
increasing  nuniljer  of  fine  fat  grainiles  may  be  observed.  At  this 
period  the  altered  medulla  occupies  a  larger  space  than  in  health,  so 
that  the  fibies  appear  broader  than  usual,  but  their  outlines  are  some- 
what irregular  and  wavy.  As  the  morbid  processes  advance  the  me- 
dulla becomes  gradually  converted  into  fat  granules,  which  are  finally 
absorbed.  The  axis-cylinder  is  said  by  some  observers  to  persist  for  a 
long  time  after  the  medullary  sheath  has  disapi)eare(l,  l)ut  Ranvier 
asserts  that  the  protoplasm  collects  at  the  level  of  the  interannular 
nucleus  to  such  an  extent  that  it  compresses,  and  finallv  intersects  the 
axis-cylinder  (Fig.  49,  3,  ;?  <•?/),  which  may  also  at  a  subsequent  period 
be  cut  across  by  the  accumulation  of  protoplasm  at  other  levels.  On 
the  fourth  day  after  section  the  nucleus,  which   is  situated  neai-   the 


DISSOLUTION    OF    THE    XERVOUS    SYSTEM.  101 

middle  of  an  interaniiular  segment,  contains  a  large  and  distinct  nucleo- 
lus (Fig.  41t,  ."),  n),  which  may  present  an  hour-glass  contraction,  or  be 
divided  into  two.  After  a  time  the  nucleus  exhibits  a  similar  trans- 
formation, and  ends  by  becoming  completely  divided  into  two  nuclei, 
each  of  which  may  subsequently  undergo  subdivision,  and  these  four 
nuclei  may  l)e  found  in  one  interannular  segment  (Fig.  49, 6,  n" n"  n" n"). 
At  a  later  ])eriod  of  the  degenerative  process  the  greater  portion  of  the 
medulla  is  absor1)ed,  although  some  globular  masses  may  accumulate  at 
certain  points  in  the  length  of  the  fibre  (Fig.  49,  6,  in),  the  process  of 
multiplication  of  nuclei  ceases,  and  even  the  axis-cylinder  disappears 
from  considerable  portions  of  the  length  of  the  fibre.  The  result  of 
this  process  is  that  the  sheath  of  Schwann  is  completely  empty  of  its 
contents  at  certain  points,  and  collapses  so  that  the  degenerated  fibre 
appears  very  slender  (Fig.  49,  a  a).  The  calibre  of  the  tube  is  dis- 
tended at  intervals  by  elongated  nuclei  arranged  in  a  series  (Fig. 
49,  9,  n  n),  by  fragments  of  the  axis-cylinder,  or  by  globular  masses  of 
altered  myeline  (Fig.  49,  9,  »?),  and  the  degenerated  nerve  tube  now 
appears  as  a  delicate  pale  band  with  irregularly  undulating  contour. 
With  the  disappearance  of  the  medullary  sheath  the  degenerated  nerve 
loses  its  white  color  and  assumes  a  gray  appearance,  the  fibres  shrink, 
and  the  nerve  looks  small  and  wasted.  This  process  is  probably  accom- 
panied Ijy  proliferation  of  the  cells  of  the  endtmeurium,  or  even  of  the 
perineurium,  and  in  long-standing  cases  the  newl}"  found  tissue  under- 
goes cicatricial  shrinking,  or  cirrhosis,  rendering  the  texture  of  the  de- 
generated  nerve  denser  and  adding  to  its  atrophied  appearance. 

(2)  Regeneratvni  of  Nerves. — Under  favorable  circumstances,  the 
process  of  dissolution  is  arrested  and  a  new  evolution  begins.  If  the 
ends  of  the  divided  nerve  are  maintained  in  apposition  during  the  repa- 
rative process,  it  is  probable  that  the  axis-cylinders  of  the  central  and 
peripheral  ends  may  become  connected  before  any  serious  degenerative 
changes  have  occurred  in  the  latter  of  the  two  segments.  But  when 
the  ends  are  not  in  apposition,  the  nerve  tubes  of  the  peripheral  seg- 
ment become  degenerated  in  their  entire  extent,  and  the  subsequent 
regeneration  is  eifected  by  an  active  growth  of  the  nerve  tubes  of  the 
central  segment.  Several  ways  are  described  by  Ranvier  in  which  the 
central  ends  give  rise  to  new  nerve  fibres,  but  only  one  or  two  of  the  more 
common  of  these  will  be  mentioned  here.  The  central  tube  terminates 
by  a  slight  enlargement  of  one  of  the  nodes  (Fig.  49,  7),  and  from  this 
extremity  a  nerve  tube  {t')  issues,  which,  although  thin,  is  furnished  by 
a  medullary  sheath  {s')  and  interannular  nucleus.  This  tube  subdivides 
into  two  others  of  almost  the  same  size  as  itself,  and  each  of  these  in 
its  turn  subdivides  into  two  new  nerve  tubes,  so  that  the  old  sheath 


102        MOEBID    ANATOMY    OF    THE    NEKYOUS    SYSTEM. 

of  Scliwann  becomes  distended  by  a  bundle  of  new  fibres  (Fig.  4<J,  7, 
F).  Rounded  masses  of  altered  myeline  {m)  are  often  observed  to  lie 
at  intervals  between  the  old  sheatli  and  the  young  fibres.  At  other 
times  several  nerve  tubes  (Fig.  49,  8,  t  t'  t"),  some  of  them  possessing 
distinct  medullary  sheaths,  while  others  consist  of  naked  axis-cylinders, 
issue  from  the  extremities  of  the  central  fibres,  and  these  also  extend 
towards  the  pei-iphery.  These  new  fibres,  on  reaching  the  peripheral 
segment,  penetrate  for  the  most  part  into  the  interior  of  the  degenerated 
tubes;  but  some  of  them,  according  to  Ranvier,  insinuate  themselves 
between  the  old  sheath  and  the  substance  of  the  endoneurium.  The 
duration  of  the  process  of  regeneration  varies  according  as  there  is 
simple  division  of  the  nerve  or  a  portion  is  resected.  It  is  also  influ- 
enced by  numerous  other  circumstances,  the  most  important  of  which 
is  the  length  of  the  peripheral  part  of  the  divided  nerve,  restoration 
being  so  much  the  slower  the  longer  that  portion  of  the  nerve  is. 
Schiif  found  complete  reunion  of  divided  nerves  in  young  animals  in 
from  seven  to  fourteen  days,  and  Paget  found  in  two  cases  of  complete 
division  of  nerves  traces  of  returning  sensibility  in  fifteen  days.  Sen- 
sory functions  are,  however,  restored  considerably  sooner  than  motor 
functions,  and,  after  division  of  the  fiicial  nerve,  the  return  of  motor 
power  in  the  facial  muscles  only  takes  place  after  the  lapse  of  two  or 
three  months.  If  a  portion  of  the  nerve  is  resected  the  process  of 
repair  takes  a  much  longer  time,  and  if  tlie  ])ortion  of  nerve  removed 
exceeds  two  inches  regeneration  is  not  likely  to  take  place.  The  nei've 
fibres  of  the  white  substance  of  the  spinal  cord  and  brain  are  found  to 
undergo  a  degeneration  essentially  similar  in  kind  to  that  just  described 
as  occurring  in  peripheral  nerves.  That  degeneration  of  nerve  fibres 
conforms  to  the  law  of  dissolution,  and  their  regeneration  to  that  of 
evolution,  is  too  obvious  to  require  pointing  out  in  detail. 

(3)  Hyjyertnyphy  of  the  Axis-cylinder. — In  myelitis  the  axis-cylin- 
ders of  many  of  the  fibres  appear  on  transverse  section  two  or  three 
times  the  normal  size,  but  it  is  seen  on  longitudinal  section  that  the 
swelling  does  not  extend  the  Avhole  length  of  the  axis-cylinder,  the 
fibre  now  presenting  a  varicose  appearance. 

(4)  Calcareous  degeneration  of  the  fibres  of  the  spinal  cord  has 
been  exceptionally  observed. 

(2)  Dissolution  of  the  Nervous  Tissues. 

The  morbid  changes  of  the  nervous  tissues  manifest  themselves  in 
(1)  the  parenchymatous  elements;  (2)  the  connective  tissue  or  neu- 
roglia ;  (3)  the  bloodvessels  ;  and  (4)  the  blood. 


DISSOLUTION    OF    THE    NERVOUS    SYSTEM.  103 

(1)  Morbid  Changes  of  Parenchymatous  Elements. 

The  morbid  changes  of  the  i)arenchyma  of  the  nervous  system  are 
the  .^^anie  as  those  ahvadv  descril)e(l  as  occurring  in  the  cells  and  fibres, 
the  kind  of  alterations  -which  take  place  depending  upon  whether  the 
process  is  acute  or  chronic,  or  it  be  caused  by  an  irritative  or  degenera- 
tive lesion,  or  upon  various  other  circumstances. 

(2)  Morbid  Changes  or  the  Neuroglia  and  Connective  Tissue. 

(a)  Hypertrophy  and  Hyperplasia  of  the  Connective  Tissue. — In 
intiammation  of  nervous  tissues  the  septa  of  the  connective  tissue 
become  swollen,  while  its  nuclei  and  those  of  the  neuroglia  are  largely 
increased  in  number.  It  is  also  probable  that  the  leucocytes,  which 
have  migrated  from  the  vessels,  may  subsequently  ])ecome  organized, 
and  thus  increase  the  volume  of  tlie  connective  tissue. 

(h)  Interstitial  Sclerosis. — When  hyperplasia  of  the  connective  tissue 
has  once  taken  place,  the  newly  formed  tissue  may  undergo  cicatricial 
contraction,  and  thus  lead  to  the  destruction  of  the  nervous  elements, 
by  a  kind  of  cirrhosis  or  interstitial  sclerosis. 

((')  G-l'dye's  Corpuscles. — These  corpuscles  ai-e  large  globular  cells 
which  are  distended  with  granular  contents ;  they  are  met  in  the 
nervous  system  of  the  embryo  in  considerable  numbers,  but  are  only 
sparsely  distributed  in  that  of  the  adult,  except  in  cases  of  disease,  and 
then  are  sup})Osed  to  be  derived  from  fatty  degeneration  of  the  cells  of 
the  connective  tissue  and  neurcjglia,  the  white  corpuscles  of  the  blood, 
and  the  endothelial  cells  of  the  capsules  of  the  ganglion  cells  of  blood- 
vessels. 

{d)  Amyloid  Corpuscles  and  Colloid  Bodies. — Amyloid  corpuscles 
(corpora  amylacea)  are  small,  round,  concentrically  laminated  bodies, 
most  of  which  turn  blue  or  bluish-gray  when  acted  on  by  iodine,  and 
assume  a  l)eautiful  blue  tint  on  the  addition  of  sulphuric  acid.  Colloid 
bodies  are  irregular  masses,  consisting  apparently  of  changed  myeline, 
and  assuming  beautiful  tints  on  being  stained  with  logwood  or  some  of 
the  aniline  dyes.  Neither  of  these  bodies  affords  trustworthy  evidence 
of  disease,  inasmuch  as  they  may  probably  result  from  post-mortem 
mortem  changes. 

(e)  Deiters  cells  appear  to  be  much  increased  in  number  in  inflam- 
matorv  diseases  of  the  nerve  centres. 

(3)  Morbid  Alterations  of  the  Vessels. 

(a)  Intravascular  Changes. — The  vessels  are  at  times  greatly  dis- 
tended with  blood,  but  this  distention  may  have  occurred  from  the  mode 
of  dying,  or  from  hypostatic  congestion  after  death. 


1(14        MOUHIl)    AXATOMY    OF    THE    XERVOUS    SYSTEM. 

{(>)  Capillar^/  Extravasations.— In  the  early  stage  of  inflammation 
of  nervous  tissues  the  affected  part  assumes  a  reddish  color,  and  lie- 
comes  studded  hx  a  number  of  capillary  extravasations,  each  about  the 
size  of  a  pin's  head,  these  being  sometimes  so  numerous  that  the  part 
presents  the  appearance  of  a  hemorrhagic  infarct. 

{<-)  Thirkemn;/  of  the  walls  of  the  vessels  of  the  nervous  system  is 
found  in  cln-onic  Bright's  disease  similar  to  that  which  occurs  in  the 
vessels  of  the  body  generally  in  that  disease. 

(d)  Perivascular  Changes. — The  most  important  perivascular  changes 
observed  in  disease  of  the  nerve  centres  are  caused  by  migration  of  the 
white  corpuscles  of  the  blood  into  the  perivascular  lymph  spaces  and 
surrounding  tissues.  The  number  of  leucocytes  surrounding  a  vessel 
may  sometimes  be  so  great  as  to  constitute  what  has  been  called  a 
miliary  ahsress. 

(e)  Atlieroina  and  Aneurism. — The  vessels  of  the  brain  are  as  sub- 
ject to  atheromatous  changes  as  those  of  the  body  generally,  and  these 
changes  are  very  prone  to  occur  in  syphilitic  subjects  at  a  comparatively 
early  age.  When  the  cerebral  arteries  are  diseased  the  smaller  branches 
often  undergo  saccular  dilatations,  which  have  been  named  by  Charcot 
)inliary  aneurisms.  They  are  said  to  lesult  from  a  kind  of  arterial 
sclerosis  of  the  nature  of  a  chronic  periarteritis,  consisting  of  multijdi- 
cation  of  the  nuclei  of  the  lymph  sheaths  and  adventitia,  with  atrophy 
of  the  muscular  coats.  These  aneurisms  ai-e  liable  to  rupture,  and 
thus  give  rise  to  massive  hemorrhages  in  the  brain.  Atheroma  of  the 
vessels  may  also  lead  to  aneurisms  of  the  medium  sizeil  and  larger 
arteries  of  the  brain,  which  may  compress  and  desti-oy  the  nervous 
substance  like  other  tumors,  or  cause  sudden  destruction  of  large  })or- 
tions  of  it  by  rupturing  and  giving  rise  to  massive  hemorrhages. 

(/)  Occlusion  of  Bloodvessels. — In  valvular  diseases  of  the  heart  a 
fibrinous  mass  may  be  washed  off  from  the  left  cavities  of  the  heart  or 
their  valves,  or  from  the  pulmonary  veins,  or  an  atheromatous  aorta, 
and  may  be  lodged  in  one  of  the  arteries  of  the  brain,  the  left  middle 
cerebral  artery  being  the  one  most  liable  to  be  occluded.  This  process 
is  termed  cmholis)n.  The  embolus  sometimes  consists  of  a  cancerous 
nodule  washed  from  the  pulmonary  vessels  in  cancer  of  the  lungs,  or  of 
a  syphilitic  nodule  which  had  projected  into  the  interior  of  one  of  the 
arteries  of  the  neck  or  brain.  A  cerebral  vessel  may  be  occliuled  l)y 
the  locid  formation  of  a  clot,  a  process  which  consti^ites  thrombosis. 

(4)  Morbid  Changes  of  the  Blood. 
In  cases  of  pysemia,  morbid  products  are  conveyed  in  the  blood,  and 
metastatic  abscesses  may  form  in  the  brain  and  other  parts  of  the  ner- 


nSSOLUTION    OF    THE    NERVOUS    SYSTEM.  105 

vous  system,  and  morbid  changes  are  apt  to  occur  in  the  nervous  tissues 
in  blood  diseases  like  anaemia,  leucocythfemia,  and  the  specific  fevei's, 
and  in  those  cases  in  -which  the  blood  contains  a  chemical  poison  like 
strvchnine,  lead,  and  alcohol. 

("))  Nem-  Formations. 

(a)  Neuromata. — Growths  in  nerves  may  be  divided  into  (j  )  true 
and  (jj  )  false  neuromata. 

( j  )  True  neuromata  consist  of  a  growth  of  nerve  fibres  mixed  with 
a  connective-tissue  formation.  True  neuromata  have  been  divided  into 
two  varieties  according  to  the  character  of  the  nerve  fibres  found  in 
them.  In  one  form  the  fibres  are  medullated,  and  consequently  it  has 
been  called  by  VirchoAv  neuroma  myelinirum ;  whilst  in  the  other  form 
the  fibres  are  non-medullated,  and  the  tumor  has  been  named  by  the 
same  author  neuroma  amyeliniewn.  True  neuromata  have  also  been 
divided  into  several  varieties  according  to  the  amount  and  character  of 
the  connective-tissue  basis  and  to  the  degree  of  vascularity,  the  more 
usual  names  applied  to  them  being  Jibro-neuroma,  glio-ncuroma,  myxo- 
neuroma.,  and  neuroma  tcleangiectodes.  True  neuromata  occur  most 
fre([uently  in  spinal  nerves,  rarely  in  sympathetic  nerves,  and  still  more 
rarely  in  one  of  the  cerebral  nerves.  They  vary  from  the  size  of  a 
millet-seed  to  that  of  the  closed  fist.  Neuromata  consisting  of  both 
gray  and  white  matter  have  occasionally  been  found  in  the  brains  of 
lunatics,  being  situated  on  the  surfiice  of  the  ventricles. 

(jj  )  False  neuromata  consist  of  tumors  of  various  kinds,  but  in 
which  there  is  no  formation  of  nerve  fibres,  these  fibres  Ijeing  indeed 
injured  or  destroyed  by  compression.  The  following  false  neuromata 
are  met  with  :  fibroma.,  often  forming  small  knots  luimed  tubercula 
dolorosa;  myxoma,  frequently  met  with  in  nerves,  and  sometimes  con- 
taining cysts,  when  they  are  called  neuroma  cysticum ;  ylioma,  found 
in  the  auditory  nerve ;  sarcoma  occurs  in  nerves,  and  transitional 
varieties  between  it  and  fibroma  and  myxoma  are  not  unfrequently 
observed :  carcinoma  occurs  occasionally  as  a  primary,  but  much  more 
frequently  as  a  secondary  growth  ;  syphilitic  gumma,  most  frequently 
found  in  the  cerebral  nerves  ;  and  lepra  nervorum  appears  as  a  difliised, 
more  or  less  fusiform  swelling  of  the  nerves. 

The  size  of  neuromata  is  extremely  variable,  being  sometimes  not 
larger  than  a  mustard-seed,  and  at  other  times  as  large  as  a  man's  head ; 
the  majority  range  between  the  size  of  a  bean  and  that  of  a  hen's  egg. 
The  number  of  the  tumors  is  as  variable  as  their  size.  In  some  cases 
there  is  only  a  solitary  tumor,  while  at  other  times  a  large  number  may 


100        MORBID    ANATOMY    OF    THE    NERVOUS    SYSTEM. 

be  present,  either  at  a  circumscribed  spot  or  distributed  over  the  body, 
the  number  in  some  cases  being  as  high  as  from  eight  hundred  to  sevei-al 
thousands. 

The  nerve  sometimes  passes  on  one  side  of  the  tumor  ;  at  other  times 
tlie  tumor  occupies  the  centre  of  the  nerve ;  while  in  other  cases  the 
nerve  runs  directly  into  the  tumor,  the  fibres  breaking  up  into  a  kind 
of  brush  or  pencil. 

(h)  Gh'oiiiata  form  tumors  which  vary  in  size  from  a  cherry-stone 
to  that  of  the  closed  fist ;  they  may  be  localized  in  any  part  of  the 
brain  or  spinal  cord,  but  are  most  frequently  found  in  the  hemispheres 
of  the  brain.  Gliomata  consist  of  a  matrix  and  an  abundant  admixture 
of  round,  oval,  or  stellate  cells  with  granular  contents  and  one  or  two 
nuclei,  the  structure  of  the  tumor  being  like  that  of  the  neuroglia. 
When  the  cells  are  abundant  the  tumor  is  soft,  vascular,  of  a  grayish- 
red  color,  and  infiltrates  into  the  nervous  tissues  :  l)ut  when  the  cells 
are  relatively  few,  and  the  matrix,  which  is  fi)rmed  of  fine  fibrillge  or  a 
dense  reticulum,  is  abundant,  the  tumor  is  Jiard,  not  very  vascular, 
white  in  color,  and  it  is  more  or  less  cii'cumscribed,  although  never 
encapsulated.  The  hard  gliomata  are  allied  in  general  characters  to 
the  fi])romata,  and  intermediate  forms  are  met  with  which  are  termed 
jibro-jiUoiimta.  Transitional  forms  are  also  observed  between  gliomata 
and  sarcomata,  named  olio-sarcomata.  \X  other  times  jjliomatous 
tumors  undergo  a  mucoid  degeneration,  and  they  then  reseml)le  myxo- 
mata;  Avhile  some  of  them  are  so  richly  sui)plied  by  bloodvessels  that 
they  have  been  named  telangiectatic  gliomata,  these  being  of  great 
importance  from  their  liability  to  hemorrhage. 

(c)  Hyjjerplasia  of  the  'pineal  (/land  is  very  similar  to  gli»mm.  It 
forms  a  solid,  grayish-red,  slightly  lobulated  tumor,  which  may  grow  to 
the  size  of  a  walnut,  or  larger.  In  old  persons  the  tumor  generally 
contains  a  large  number  of  sand-like  bodies. 

(d)  Myxomata  take  their  origin,  like  gliomata,  from  an  overgrowth 
of  the  neuroglia,  but  are  }-arer  in  the  brain  tlian  in  the  spinal  cord  and 
periphei'al  nerves. 

{e)  Solitary  tuhcrde  forms  a  hard,  rounded  nodule,  which  varies  from 
the  size  of  a  pea  to  that  of  a  pigeon's  egg,  and,  on  section,  the  interior 
IS  seen  to  be  yellowish  and  cheesy ;  while  the  outer  cortex,  which  is 
only  about  a  line  in  thickness,  is  of  a  reddish-gray  color,  and  very 
vascular.  These  tumors  are  met  with  in  all  parts  of  the  brain,  but 
then-  favorite  seat  is  the  cortical  substance  of  the  cerebrum  and  cere- 
bellum, close  upon  the  cortico-medullary  boundary.  It  is  also  one  of 
the  most  fre(|uent  forms  of  tumor  met  with  in  the  spinal  cord.     Tliis 


DISSOLUTION    OF    THE    XERVOUS    SYSTEM.  107 

ruiiiov  is  often  imilti])le,  but  Avlieii  it  is  solitary  it  may  attain  a  consider- 
able size. 

(f)  CarcinoiUKtd  may  gioAv  on  the  outer  surface  of  tlie  dura  mater, 
and,  ultimately  perforating  the  bones  of  the  skull,  form  fungus  lucma- 
todes  of  the  dura  mater.  It  may  also  grow  from  the  under  surface  of 
the  pia  mater,  and  the  growth  may  then  be  primary  or  secondary  ;  but 
primary  cancer  in  this  situation  is  the  more  common  of  the  two.  Can- 
cerous tumors  of  the  brain  may  be  single  or  multiple.  They  destroy 
the  neighboring  tissues  by  pressure  and  infiltration,  and  are  usually 
suri'ounded  by  a  zone  of  softened  tissue,  of  about  a  line  in  breadth,  in 
which  active  growth  proceeds. 

(//)  Cholesteatoma,  or  })earl  cancer,  appears  to  be  derived  from  the 
l)ia  mater,  and  is  usually  situated  in  some  hollow  at  the  base  of  the 
brain.  The  tumor,  on  section,  is  hard,  pearly,  non-vascular,  and  com- 
posed of  epidermic  cells,  arranged  in  concentric  layers,  which  have 
undergone  partly  horny  and  partly  fatty  degeneration.  The  tumor  is 
enclosed  in  a  delicate  fibrous  capsule,  and  its  surface  presents  a  beautiful 
mother-of-])earl  lustre.  These  tumors  grow  very  slowly,  and  may  remain 
for  a  long  time  without  giving  rise  to  symptoms. 

(//)  Papilloma  of  the  cere])ral  pia  mater  is  occasionally  met  with. 

(^)  Syp1nlomat((  may  reach  the  size  of  a  walnut  or  of  a  hen's  egg, 
and  are  usually  found  near  the  surface  of  the  brain,  developing  from 
the  perivascular  sheaths.  They  are  only  met  with  in  the  cord  on  rare 
occasions. 

{k)  Sarco)nata  aj)j)ear  as  hard,  slightly  vascidar,  round,  somewhat 
nodulated  tumors.  Every  variety  of  sarcoma  is  found  in  the  brain, 
and  transitional  forms  between  sarcoma  and  other  tumors  are  named 
fflio-sarcoma,  myxosarcoma,  etc.  In  some  of  the  spindle-celled  sar- 
comas the  cells  are  arranged  in  concentric  layers  or  nests,  and  conse- 
quently this  form  has  been  named  "nested  sarcoma." 

(?)  Melanoma  is  a  pigmented  sarcomatous  tumor  Avhich  springs  from 
the  pigment  cells  of  the  pia  mater. 

(m)  Lipoma  has  occasionally  been  met  with  on  the  inner  surface  of 
the  dura  mater,  and  the  raphe  of  the  corpus  callosum,  and  the  fornix. 

in)  Psammomum  is  a  tumor  with  a  basis  of  connective  tissue,  or 
sometimes  of  mucoid  tissue,  which  is  distinguished  by  containing  calca- 
reous concretions.  It  appears  to  be  a  calcareous  deposit  in  tumors  of 
widely  different  structure,  the  most  frequent  of  these  being  nested 
sarcoma. 

(o)   Osteomata  are  the  rarest  of  all  intracranial  growths. 

(p)  Cystic  growths  are  caused  1:)y  a  portion  of  the  posterior  cornu 
of  the  lateral  ventricle  l)eing  cut  off  from  the  general  cavity  by  dropsy 


108        MORr.ID    ANATOMY    OF    THE    XERVOUS    SYSTEM. 

of  the  septum  lucidum,   and  cystic  degeneration  of  the  pineal   gland 
and  pituitary  body,  and  gliomatous  tumors. 

(r)  Angiomata  generally  occur  in  the  l)rain  as  a  complication  of 
other  tumors  such  as  glioma.     Pachymengitis  hc\?morrhagica  belongs  to 

this  class. 

(6)  Ankurism. 

Aneurisms  of  the  larger  cerebral  vessels  are  not  very  rare,  and  when 
they  attain  to  a  considerable  size  they  give  rise  to  the  usual  symptoms 
of  an  intracranial  growth. 

(7)  Parasites  or  thp:  Brain. 

[a)  Cysticcrcus  cellulosa  is  met  with  in  the  parts  of  tlie  l)rain  which 
are  richly  supplied  with  blood,  and  the  parasite  is  sometimes  found  in 
other  parts  of  the  body  as  well  as  in  the  brain.  Cerebral  cysticerci 
are  usually  enclosed  in  a  soft  capsule,  in  which  the  animal  may  be  seen 
with  the  naked  eye  as  a  small  tubercle,  and  its  neck,  with  the  charac- 
teristic booklets,  may  be  discovered  on  microscopic  examination. 

(b)  Echinococcus  hominis  form  cysts  Avhich  often  attain  to  a  large 
size  in  the  brain.  In  a  case  reported  by  Dr.  Morgan  the  cyst  Aveighed 
eighteen  and  a  half  ounces,  and  contained  eighteen  ounces  of  serum. 
They  reach  their  greatest  size  in  the  hemispheres  and  the  ventricles, 
especially  in  children  before  the  foutanelles  are  closed.  The  cyst  is 
composed  of  an  external  fibrous  membrane,  which  encloses  the  para- 
sites ;  its  internal  surfice  is  lined  l)y  small  l)uds,  each  about  the  size  of 
a  millet-seed,  which  are  provided  with  the  characteristic  ring  of  booklets. 


o.  Dissolution  of  thk  Nervous  System  {continued). 

a.  3fassive  HcmorrJiagcs. 

Massive  hemorrhages  generally  destroy  a  considerable  portion  of  the 
nervous  system.  In  the  recent  condition  the  apoplectic  focus  forms  a 
dark  red  soft  clot,  which  is  frequently  mixed  wdth  the  debris  of  the 
brain  substance.  The  internal  surfiice  of  the  cavity  is  irregular  and 
consists  of  torn  shreds  of  cerebral  tissue,  and  it  is  surrounded  ])y  a 
zone  of  variable  thickness  in  which  the  tissue  is  softened  by  the  inhibi- 
tion of  serum,  and  in  which  numerous  punctiform  hemorrhages  are 
observed.  If  the  patient  survives,  the  tissues  surrounding  the  blood- 
clot  become  softened  partly  by  the  imbibition  of  serum  and  partly  from 
a  retrograde  fatty  metamorphosis  of  the  torn  fragments  of  brain  tissue, 
and  the  softened  tissues,  when  mixed  up  with  the  blood  clot,  form  a 


DISSOLUTION    OF    THE    NERVOUS    SYSTEM.  109 

dark  cliocolate-i-olored  mass  of  the  consistence  of  gruel.  The  hcematin 
uoAv  becomes  grachially  absorbed,  and  the  substance  filling  the  cavity 
changes  to  a  brighter  red  or  saffron  color.  After  a  time  a  fibrous  cap- 
sule forms  round  the  clot,  and  the  solid  constituent  becoming  absorbed, 
a  cyst  is  formed  -which  contains  at  first  a  turbid,  and  subsequently  a 
clear,  limjjid,  or  straAv-colored  fluid,  having  frequently  suspended  in  it 
a  film  of  loose  spongy  connective  tissue.  When  the  cyst  is  small,  and 
the  fluid  is  absorbed,  the  opposite  walls  may  come  in  contact  and 
mlhere  by  a  connective  tissue,  -which  usually  contains  a  considerable 
amount  of  pigment,  and  gives  rise  to  the  appearance  known  as  the 
a|)()plectic  or  hemorrhagic  cicatrix. 

h.  Jlorbid  Changes  caused  by  Occlusion  of  Bloodvessels. 

^Vhen  a  terminal  artery  becomes  occluded  the  arterioles  and  vessels 
of  the  ])art  are  imperfectly  nourished,  and  consequently  their  walls 
dilate  and  fre<|uently  rupture,  the  former  causing  redema  and  the  latter 
hemorrhage.  The  softened  tissues  are  named  red,  yellow,  or  white 
softening  according  as  a  considerable  amount,  a  moderate  amount,  or 
no  1)lood  is  extravasated  from  the  vessels. 

e.  Morbid  Clianges  caused  by  Thickening  of  the  Walls  of  the 

Arterioles. 

The  walls  of  the  Ijloodvessels  of  the  nerve  centres  become  thickened 
in  Brights  disease,  and  the  nervous  tissues  surrounding  the  altered 
vessels  undergo,  in  some  cases,  morbid  changes  more  or  less  similar  to 
those  of  chronic  inflammation,  and  consisting  of  an  increase  of  connec- 
tive tissue  and  destruction  of  nerve  cells.  This  condition  may  be 
named  vascular  sclerosis. 

d.  Inflammation  of  the  Nervous  System. 

(1)  Acute  inflammation  of  nervous  tissues  is  characterized  in  its  first 
stage  by  congestion,  capillary  extravasations,  and  some  oedema  of  the 
tissues.  If  the  ju'ocess  proceeds  further,  it  causes  softening  of  the 
inflamed  part.  Inflammatory  softening  may  be  divided  into  (a)  red, 
{b)  yellow,  (c)  white,  {d)  gray,  and  ie)  green  or  purulent  softening. 

[a)  Red  Softening. — The  spot  affected  with  red  softening  is  soft, 
and  swells  up  aljove  the  level  of  the  surrounding  surface  on  section. 
The  aflected  tissue  may  be  washed  away  by  a  gentle  stream  of  water, 
or  it  may  be  diflHuent.  Numerous  capillary  hemorrhages  may  be  ob- 
served, and  the  aflected  part  assumes  a  tint  which  varies  from  rosy  to 
deep  red,  reddish-broAvn,  or  chocolate. 


11(1        M(.KIUI)    ANATOMY    OF    THE    XEKVOUS    SYSTEM. 

(//)  Yellow  Softenhu/.—A^  tlie  disease  progresses  the  affected  parts 
l.t'coiiie  i)aler  and  softer,  and  the  color  changes  to  veHow.  partly  from 
diffusion  and  alteration  of  the  coloring  matter  of  the  Idood,  and  partly 
from  degeneration  of  the  medullary  sheath. 

{<■)  White  Softniinij. — Owing  to  the  continued  process  of  fatty  de- 
generation the  color  hecomes  progressively  whiter,  and  the  diseased 
portions  assume  a  creamy  oi-  milky  appearance,  and  on  section  the 
medulla  swells  up  ahove  the  surface  of  the  surrounding  tissues. 

{d)  Gray  Softening. — In  consequence  of  the  absorption  of  fat  gran- 
ules and  nerve  substance,  the  affected  part  gradually  assumes  a  grayish 
eolor,  and  finally  becomes  smaller  and  more  depressed  than  normal. 

{e)  Green  Softenim/. — The  white  blood-corpuscles  may  migrate  in 
such  large  numbers  that  the  affected  ])art  is  converted  into  a  cavity 
containing  a  greenish  purulent  fluid,  and  constituting  an  abscess. 

Microscopical  Cha)u/es. — In  the  early  stage  of  inflammation  the 
arterioles  and  capillaries  are  dilated  and  distended  with  blood,  while 
they  may  be  enveloped  in  layers  of  migrated  white  and  red  blood- 
corpuscles.  As  the  disease  advances  the  walls  of  the  vessels  become 
tliiekened  and  studded  with  fat  granules  and  granule  cells,  Avhile  the 
lymph  sheaths  are  tilled  with  granular  or  cellular  exudation.  The  reti- 
culum of  the  neuroglia  is  swollen  and  thickened,  and  filled  with  nuclei, 
lymphoid  cells,  and  granule  cells,  while  Deiters  cells  are  increased  in 
number.  The  nerve  fibres  present  irregular  contractions  and  enlarge- 
ments, the  medullarv  sheath  becomes  broken  down  into  globules  and 
is  finallv  absorbed,  and  the  axis-cvlinders  are  greatly  swollen,  while  in 
the  second  stage  the  medullarv  sheaths  are  in  a  state  of  fattv  degenera- 
tion,  and  the  axis-cylinders  are  altered  or  destroyed.  The  ganglion 
cells  are  first  swollen,  the  nucleus  and  nucleolus  may  l)e  observed  in 
process  of  division,  while  at  other  times  they  undergo  vacuolation,  the 
cell  processes  are  swollen,  cloudy,  irregular  in  shape,  and  partly  de- 
stroyed, and  at  a  later  period  the  cells  lose  their  processes,  and  shrivel 
so  as  to  become-  reduced  to  small  angular  masses  without  structure. 
When  a  cicatrix  has  formed,  the  affected  spot  is  occupied  by  a  dense 
connective  tissue  containing  many  nuclei  and  neuroglia  cells,  and  numer- 
ous Deiter's  cells.  When  cijsts  are  formed  they  are  surrounded  by  a 
more  or  less  dense  layer  of  connective  tissue,  and  are  generally  trav- 
ersed by  a  loose  connective-tissue  network. 

The  morbid  appearances  just  described  apply  more  particularly  to 
those  occurring  in  the  spinal  cord  and  termed'  ctcute  myelitis,  and  in 
the  brain  and  named  acute  encephalitis,  l)ut  essentially  the  same 
changes  are  met  with  in  acute  inflammation  of  nerves.  When  the 
inflammation  begins  in  the  nerve  fibres  the  process  is  named  neuritis, 


DISSOLUTIOX    OF    THE    NERVOUS    SYSTEM.  lU 

and  when  in  the  slieath  of  the  nerve  it  is  named  perineuritis.  In  acute 
neuritis  or  periaeuritis  the  vessels  become  enhu-ged  and  distended,  and 
the  nerve-trunk  is  swollen  from  serous,  gelatinous,  or  fibrinous  exudation. 
If  the  inflammation  subside  at  ari  early  date  the  effusion  is  absorbed 
l)efore  there  is  any  destruction  of  the  nerve  fil)res,  and  the  healthy 
condition  is  reestablished.  If  the  inflammatory  action  is  very  acute 
and  severe,  both  white  and  red  corpuscles  escape  from  the  vessels,  the 
color  of  the  nerve  l)ec()mes  yellow  or  brownish-red,  its  tissues  are  infil- 
trated with  sanguineous  pus,  abscesses  may  form  around  its  trunk,  and 
the  entire  structure  may  l)ecome  completely  disintegrated. 

(2)  Chronic  inpmimation  causes  the  aifected  part,  as  a  rule,  to  be 
atrophied,  and  unusually  dense  or  in  a  state  of  sclerosis.  When  the 
white  substance  is  the  subject  of  chronic  inflammation  it  assumes  a  gray 
color,  and  consequently  the  condition  is  sometimes  called  (p'iiy  degene- 
ration. When  the  inflammation  spreads  over  a  considerable  area  of 
tissue  it  is  named  diffused  sclerosis  ;  when  it  is  limited  to  the  embrvo- 
logical  tracts  of  the  cord  it  is  named  an  ascending  or  a  descending 
sclerosis,  according  as  the  process  extends  from  below  upwards  oi-  from 
above  downwards  ;  when  it  is  limited  to  certain  spots  or  foci  it  is  named 
circumscribed  or  insular  sclerosis ;  and  when  these  spots  are  numerous 
and  distributed  in  diff"erent  parts  of  the  nervous  system,  it  is  named 
multiple  or  dissoninated  sclerosis.  The  terms  insular,  multiple,  and 
disseminated  are  applied  indiff'erently  to  the  same  disease,  because,  when 
the  sclerosis  is  limited  to  circumscribed  spots,  the  spots  are  also  mul- 
tiple and  widely  distributed  over  the  nervous  system.  When  the 
sclerosis  is  more  or  less  restricted  to  the  embryological  tracts  the 
morbid  process  is  supposed  to  begin  in  the  nervous  elements  themselves, 
and  consequently  some  anatomists  have  called  this  form  of  chronic 
inflammation  parencliymatous  sclerosis.  This  distinction  is  admissible 
theoretically,  l)ut  it  is  not  always  easy  to  maintain  it  practically.  A 
microscopical  examination  of  a  part  in  a  state  of  sclerosis  shows  that 
the  connective-tissue  septa  are  thickened,  and  that  the  cells  of  the  neu- 
roglia are  swollen  and  their  nuclei  multiplied.  Deiters  cells  are  also 
increased  in  size  and  number,  and  in  long-standing  cases  the  neuroglia 
becomes  converted  into  a  dense  fibrillated  connective  tissue  in  which  a 
large  number  of  nuclei  are  observed.  The  nerve  fibres  undergo  changes 
more  or  less  similar  to  those  which  occur  in  secondary  degeneration  of 
the  fibres  of  the  peripheral  nerves.  The  medullary  sheath  undergoes 
granular  and  fatty  degeneration,  and  is  finally  absorbed ;  but  the  axis- 
cylinder  persists  a  long  time,  although  it  becomes  swollen  at  certain 
points,  and,  on  being  viewed  longitudinally,  presents  spindle-shaped 
enlargements.    After  a  time  the  axis-cvlinders  also  Avaste  and  disappeai\ 


[[•1        MOHHID    AXATOMY    OF    THE    NEEVOUS    SYSTEM. 

and  nothing-  remains  l»ut  a  dciise  fil)i'illate(l  connective  ti^^ue.  The 
ualls  of  the  small  arteries  and  veins  become  thickened,  and  their  calibre 
is  diminished  in  size.  The  lymph  spaces  are  destroyed,  or  contain  fat 
and  jiigment  granules,  while  granule  cells  and  corpora  amylacea  are 
found  scattered  through  the  diseased  tissue. 

The  morbid  apjiearances  just  described  are  met  with  in  the  nervous 
centres,  but  essentially  similar  alterations  occur  in  nerves.  In  chronic 
neuritis  and  perineuritis  the  trunk  of  the  nerve  becomes  irregularly 
vascular,  and  is  enlai-ged  in  some  places  and  atrophied  in  others.  The 
sheath  of  the  nerve  is  thickened,  fibrous,  and  resisting,  while  it  is  fre- 
(|uentlv  adherent  to  the  adjacent  tissues.  In  cases  of  perineuritis  the 
nerve  filtres  are  compressed  by  the  exudation  and  disappear  after  a 
time,  so  that  tlie  sti'ucture  of  the  nerve  is  supplanted  by  a  band  of 
connective  tissue. 

Segmental  periaxillary  neuritis,  induced  l)y  Gombault  in  the  perij)h- 
eral  nerves  of  guinea-pigs,  is  a  parenchymatous  neuritis  in  which  only 
a  part  of  the  nerve  fibre  is  implicated.  A  segment  lying  between  two 
of  the  nodes  of  Ranvier  is  diseased,  while  those  on  each  side  of  it  may 
remain  healthy.  Several  seginents  may,  however,  be  affected  in  the 
course  of  one  fibre.  The  medullary  sheath  and  the  protoplasm  of  the 
fibre  are  at  fii-st  alone  implicated  in  the  morbid  change,  while  the  axis- 
cylinder  remains  for  a  long  time  uninterrupted.  After  a  time  the 
diseased  segment  may  either  be  restored  by  the  growth  of  a  new  medul- 
lary sheath,  or  the  axis-cylinder  becomes  ruptured,  and  the  ])eripheral 
end  of  the  nerve  then  undergoes  the  Wallerian  degeneration. 

e.  Degenerations  of  the  Nervous  System. 

(1)  Primary  Degeneration. 

Tlie  gray  substance  of  the  nervous  system  may  apparently  undergo 
a  primary  chronic  degeneration  in  addition  to  the  degeneration  which 
is  consecutive  to  inflammation.  In  the  primary  degeneration  the  nerve 
cells  undergo  atrophy  and  various  forms  of  ])igmentarv  defeneration. 
This  form  of  degeneration  occurs  most  probably  in  the  gray  substance 
of  the  anterior  horns  of  the  spinal  cord  in  progressive  muscular  atrophy, 
and  in  the  cortex  of  the  brain  in  the  chronic  forms  of  insanity.  It  is 
possiVde  that  the  white  substance  may  also  undergo  a  primary  chronic 
degeneration,  and  the  disease  known  as  progressive  multiple  neuritis 
appears  to  be  a  primary  degeneration  of  the  peripheral  nerves.  The 
morbid  changes  which  have  been  found  in  the  nerves  in  this  disease 
consist  of  partial  or  complete  destruction  of  many  of  the  nerve  fibres. 
The  perineurium  of  the  individual  bundles  has  also  been  found  thick- 


DISSOLUTION    OF    THE    NERVOUS    SYSTEM.  118 

ened,  and  Levden  has  observed  an  accumulation  of  fat  cells  between 
the  bundles,  and  a  deposit  of  pigment  around  the  bloodvessels.  Lev- 
den regards  this  pigment  as  a  hemorrhagic  inflammation  of  the  tissues 
between  the  nerve  fibres,  and  he  believes  that  the  absence  of  any  sio-n 
of  multiplication  of  nuclei  proves  that  the  nerve  fibres  had  become 
atrophied  through  the  compression  caused  by  the  congestion  of  the 
tissues  surrounding  them. 

(2)  Secondary  Degenerations. 

The  Wallerian  degeneration  of  peripheral  nerves  has  already  been 
described,  but  we  have  now  to  point  out  that  essentially  the  same  pro- 
cess occurs  in  the  conducting  paths  of  the  nerve  centres.  It  has 
already  been  stated  that  Waller  observed  that  when  a  mixed  nerve  is 
divided  the  peripheral  portion  degenerates  throughout  its  whole  course 
in  a  few  weeks,  Avhile  the  portion  attached  to  the  cord  does  not  degen- 
erate. This  statement,  however,  is  only  a  portion  of  the  truth.  He 
also  found  that  while  the  efferent  fibres  degenerate  their  whole  length 
on  division  of  the  anterior  root,  that  the  peripheral  portion  of  the 
afferent  fibres  do  not  degenerate  on  division  of  the  posterior  roots.  On 
division  of  the  posterior  roots  what  takes  place  is  that  the  peripheral 
portions  which  are  attached  to  the  spinal  ganglion  remain  healthy,  but 
the  small  central  portion  which  is  attached  to  the  cord  soon  wastes. 
From  these  facts  Waller  concluded  that  the  efferent  fibres  receive  their 
nutritive  influence  from  the  caudate  cells  of  the  anterior  horns,  and  the 
afferent  fibi'os  from  the  ganglia  of  the  |)OSterior  roots,  and  he  then 
formulated  the  general  law  that  nen'e  fibres  ilegenerate  when  they  are 
se])arated  fi'om  their  trophic  centres. 

The  central  conducting  paths  also  undergo  degeneration  in  one  direc- 
tion after  division  or  injury  of  them,  and  it  may  be  confidently  asserted 
that  the  degeneration  occurs  along  the  line  of  conduction  of  the  fibres,  some 
paths  undergoing  an  ascendinf/  and  others  a  di'scending  degeneration. 

(a)    ASCENDING    DEGENERATIONS. 

The  trophic  centres  of  the  columns  of  (roll  and  of  the  direct  cere- 
bellar tracts  are  situated  at  their  inferior  extremities,  the  ganglia  of 
the  })osterior  roots  or  the  gray  substance  of  the  posterior  horns  forming 
the  trophic  centres  of  the  former,  and  the  cells  of  the  vesicular  colunms 
of  Clarke  probably  those  of  the  latter.  The  lower  limit  of  the  de- 
generation of  these  columns  will  depend  upon  the  position  of  the  lesion 
of  the  cord  which  interrupts  the  continuity  of  the  fibres,  and  the 
deoeneration  of  the  columns  of   Goll    may  extentl    from    the  lumbar 

8 


114        MORHII)    ANATOMY    OF    THE    XERVOUS    SYSTEM, 


region  of  the  cord  up  to  tlie  termination  of  the  fibres  in  the  cuneate 
nucleus,  while  the  degeneration  of  the  direct  cerebellar  tracts  may 
extenil  from  the  inferior  part  of  the  dorsal  region  up  to  the  external 
surface  of  the  restiform  bodies.  In  both  of  these  degenerations  the  dis- 
eased area  increases  progressively  in  size  from  below  upwards  (Figs. 
50,  51,  5:2).     A  case  is  reported  by  Dr.  Gowers  in  which  the  lower 


Fig.  50. 


Fig.  51. 


TnANSVERsE  Sections  op  the  Spinal  Cord,   fro-ai    the  middle  of  the   Cervical  Enlargement, 

MIDDLE  OF  THE  DoRSAL  RF-GION,  AND  MIDDLE  OF  THE  LUMBAB  EEGION,  RESPECTIVELY,  SHOWING  ASCEND- 
ING Degeneration  of  the  Cdlvmns  of  Goi.L(g),  and  op  the  direct  Cerebellar  Tract  (dc). 

extremity  of  the  spinal  cord  was  crushed  by  a  fracture  of  the  spine, 
and  in  which,  in  addition  to  the  ascending  degeneration  of  the  columns 
of  Goll,  a  small  area  of  degeneration  w^as  observed  in  each  anterior 
root-zone  in  front  of  the  lateral  pyramidal  tract,  the  latter  being 
healthy  on  each  side.  Dr.  Gowers  suggests  that  these  areas  constitute 
a  part  of  the  sensory  conducting  paths.  In  lesions  of  the  cauda 
equina,  and  sometimes  after  severe  traumatic  injuries  of  the  sciatic 
nerve,  the  posterior  root-zones  as  well  as  the  columns  of  Goll  undergo 
ascending  degeneration  in  the  lumbar  and  greater  portion  of  the  dorsal 
regions,  but  the  degeneration  becomes  limited  to  the  columns  of  Goll  in 
the  upper  dorsal  and  cervical  regions.  In  transverse  lesions  of  the 
cord  the  posterior  root-zones  may  also  be  found  degenerated  for  a  short 
distance  above  the  lesion,  but  the  evidence  of  degeneration  soon  ceases, 
probably  because  the  fibres  of  these  columns  soon  tei-minate  in  gray 
matter. 

{())    DESCENDING    DEGENERATION. 

(j)  Sclerosis  of  the  Pyramidal  Tract. 
Lesions  of  the  cortex  of  the  brain,  provided  the  whole  thickness  of 
the  gray  substance  is  implicated,  are  followed  by  descending  degenera- 
tion of  the  fibres  of  the  pyramidal  tract  Avhich  may  be  followed  tiirough 
the  internal  capsule,  crusta,  longitudinal  fibres  of  the  pons,  anterior 
pyramids  of  the  medulla  oblongata  on  the  anterior  column  of  the  same 
side  as  the  lesion,  and  in  the  lateral  columns  of  the  cord  on  the  side 
opposite  the  lesion.  A  descending  degeneration  of  this  kind  has  also 
been  found  in  animals  after  extirpation  of  portions  of  the  motor  area 
of  the  cortex  of  the  brain. 


DISSOLUTIOX    OF    THE    NERVOUS    SYSTEM. 


115 


A  focal  lesion  limited  to  the  middle  third  of  the  internal  capsule 
(F\<s.  08,  F)  is  followed  by  descending  degeneration  of  the  fibres  of  the 
middle  third  of  the  crusta  (Fig.  54,  D),  and  of  a  portion  of  the  longi- 
tudinal fibres  of  the  pons  and  the  anterior  pyramid  of  the  medulla  on 
the  same  side.  The  greater  part  of  the  degenerated  fibres  cross  over 
at  the  lower  end  of  the  medulla  oblongata  to  reach  the  lateral  column 
f)f  the  opposite  side  of  the  cord  (Figs.  55,  56,  57),  while  a  few  of  them 
pass  doAvn  the  column  of  Tiirck  on  the  same  side. 


Fio.  53. 


H'liiizoxTAL  Section  of  the  Eight  Hejiisphere  Parallel  with  the  Fissuke  of  Sylviu;s.    (Charcot.) 
Xc,  Caudate  nucleus ;  Sa,  Anterior  segment  of  the  internal  capsule ;  Nl,  Lenticular  nucleus  ;  G,  Knee 
of  the  internal  capsule ;  Sp,  Posterior  segment  of  the  internal  capsule ;  Co,  Optic  thalamus ;  F,  A  focal 
lesion  in  the  middle  third  of  the  posterior  part  of  the  internal  capsule. 

In  diseases  of  the  spinal  cord  the  degeneration  is  generally  bilateral 
and  symmetrical,  and  the  positions  occupied  by  the  diseased  areas  at 
different  levels  of  the  cord  are  represented  in  Figs.  58,  59,  60.  When 
the  disease  reaches  to  the  medulla  oblongata,  the  areas  of  degeneration 
are  limited  to  the  anterior  pyramids. 

The  portions  of  the  pyramidal  tracts  which  belong  to  the  nuclei  of 


lie.   MORBID  ANATOMY  OF  THE  NERVOUS  SYSTEM. 

the  medulla  ol)l()ngata  ami  pons  are  sometimes  diseased  in  the  absence 
of  any  affection  of  the  spinal  pyramidal  tracts. 

(jj )  De<ieneration  of  the  Fillet  and  Superior  Peduncle  of  the  Cerebellum. 
In  a  case  reported  by  Homen,  a  focus  of  softening  was  found  in  the 
lateral  half  of  the  upper  part  of  the  pons,  and  the  pyramidal  tract  of 

Fig   54 


F  L  n 

Horizontal  Section  of  the  Crura  Cerebri  in  a  case  or  Secondary  Degeneration.    (Charcot  ) 
T,  Tegmentum  ;  F,  Crusta  of  the  healthy  side ;  L,  Locus  uiger  ;   D,  The  degenerated  fibres,  occiii),viug 
alidut  the  middle  third  of  the  crusta ;  P,  The  fibres  which  undergo  secondary  degeneration  imly  when  the 
fibres  (if  the  anterior  segment  and  the  knee  of  the  internal  capsule  are  diseased 

that  side  was  degenerated  below  the  seat  of  the  lesion  as  far  as  to  the 
lower  end  of  the  medulla  oblongata,  the  streak  of  deo;eneration  being 


Fig.  55. 


Fig.  5fi 


Transverse  Sections   oe  the  Spinal  Coed,  from  the   middle  of  the  Cervical  Enlargement, 

MIDDLE  of  the  DoHSAL  EEGION,  AND  MIDDLE  OF  THE  LUMBAR  KEGION,  RESPECTIVELY,  SHOWING  DE- 
SCENDING Sclerosis  of  the  Pyramidal  Tract  in  the  L.a.teral  Column  Secondary  to  a  Terebral 
Lesion.    (Charcot  ) 

.\,  .\,  A,  Degenerated  pyramidal  tracts. 

found  in  the  part  which  lies  to  the  inner  side  of  the  olivary  body.  In 
a  case  reported  by  Meyer,  a  focus  of  softening  was  found  in  the  lateral 
half  of  the  lower  part  of  the  pons,  which  embraced  tlie  nucleus  of  the 


DISSOLUTIOX    OF    THE    NERVOUS    SYSTEM. 


117 


sixth  nerve,  the  foniiatio  reticularis,  and  the  superior  olivary  body. 
Below  the  level  of  the  lesion  the  internal  division  of  the  fillet  and  the 
olivary  body  were  degenerated.     The  degeneration  of  the  fillet  could 


Fig.  58 


Fig.  50. 


Fig.  60. 


Traxsveuse  Sections  of  the  Spinal  Cord,  from  the  middle  of  the  Cervical  Enlarokment,  middle 
OF  THE  Dorsal  Region,  and  middle  of  the  Lumbar  Region,  respectively,  showing  Primary  Lateral 
Sclerosis  of  the  Cokd,  or  Secondary  to  a  Lesion  high  up  in  the  Cord  or  Medulla  Oblongata. 
(Charcot.) 

A,  A,  A,  Pegenerated  pyramiilal  tracts. 

be  traced  as  far  as  the  level  of  the  decussation  of  the  pyramidal  tract, 
and  it  was  represented  immediately  below  this  level  by  a  small  spot  of 
degeneration  near  the  periphery  of  the  external  division  of  the  anterior 

Fig.  61. 


Recent  Softening  of  the  Frontal  Lobe,  the  Island  op  Reil,  and  Middle  Third  of  the 

Lenticular  Nucleus.    (Brissaud  ) 

D,  GUI  focus  of  softening  occupying  the  knee  of  the  internal  capsule  ;  A,  Caudate  nucleus  ;  B,  Optic 

thalamus  ;  C,  Anterior,  and  E,  Posterior  division  of  the  internal  capsule. 

root-zone,  immediately  behind  the  anterior  nerve  roots.  Above  the 
level  of  the  lesion  a  secondary  degeneration  of  the  fillet  could  be  traced 
as  far  as  the  posterior  tubercle  of  the  corpora  quadrigemina. 


118        MOKBU.    ANATOMY    OF    THE   NEEVOUS    SYSTEM. 

A  case  lias  been  described  bv  Brissaud  in  whicb,  along  with  exten- 
sive recent  softening  of  one  hemisphere,  an  ohl  focus  of  softening  was 
observed  limited  exactly  to  the  knee  of  the  internal  capsule  (Fig.  bl, 
D)  A  streak  of  degeneration  was  observed  lying  between  the  internal 
and  middle  thir.ls  of  the  crusta,  being  the  anterior  portion  of  the  area 
which  has  alreadv  been  described  as  the  mixed  area  of  medullated  and 
non-medullated  fibres  in  a  nine  months'  embryo.  According  to  Bris- 
saud, degeneration  occurs  in  the  knee  of  the  internal  capsule  in  cases 
of  long-standing  aphasia. 

Fig.  r,2. 


A,  Caudate  nucleus;  B,  Optic  thalamus;  C,  Posterior  iiml  licaltliy  part  of  the  lenticular  nucleus;  D, 
Posterior  segment  of  the  internal  capsule ;  E,  Lesion  of  the  anterior  segment  of  tlie  capsule  ;  F,  ( 'yst 
presenting  the  form  of  the  lenticuhir  nucleus ;  P,  Degeneration  of  the  internal  fibres  of  the  crusta. 
(Brissaud.) 

Another  important  case  has  been  observed  by  Brissaud,  in  Avhich  an 
old  focus  of  softening  was  found  in  the  anterior  half  of  the  lenticular 
nucleus,  destroying  also  the  anterior  segment  of  tlie  internal  capsule 
(Fig.  62,  F),  A  streak  of  degeneration  was  observed  in  the  internal 
third  of  the  crusta  (Fig.  62,  P),  but  all  the  fibres  of  this  area  were  not 
implicated  in  the  degeneration,  a  small  bundle  of  tlie  innermost  fibres 


DISSOLUTION    OF    THE    XERVOL'S    SYSTEM. 


119 


remaining  normal.  The  degenerated  fibres  in  this  case  corresponded 
very  nearly  to  those  which  we  have  described  as  the  accessory  fibres  of 
the  tract.  Degeneration  of  the  internal  tract  of  the  crusta,  accordin^j; 
to  Brissaud,  appears  to  beahvays  connected  with  intellectual  disorders. 
It  is  important  to  remember  that  a  fcAv  cases  have  been  reported  of 
destructive  lesions  localized  in  the  motor  area  of  the  cerebral  hemi- 
spheres, but  in  which  no  secondary  degenerations  Avere  discovered  in 
the  internal  capsule,  crura,  pons,  medulla  oblongata,  or  spinal  cord. 

Fig.  C,?,. 


Th.o.^ 


Herd 


DiAiiEAM  OF  THE  Ol'TK    TlIALAMI,  TEGMENTUM,  ANT)  SvPEaiOR  PehUXCLES  OF  THE  ( 'EHEBEI.LVM. 

(After  Mendel  ) 

3V.,  The  third  ventricle;  Th.o.,  The  optic  thalamus;  S.t,  The  red  nucleus  of  the  tegmentum;  B., 

Superior  peduncle  of  the  cerebellum  :   C.d.,   Corpus  dentatum  of  the  cerebellum ;    Herd,   The  diseased 

focus.     The  dark  line  between  the  diseased  focus  and  the  corpus  dentatum  of  the  opposite  side  represents 

the  streak  of  degeneration. 

The  following  bundles  of  fibres  may,  therefore,  be  distinguished  in 
the  internal  capsule : 

(1)  A  posterior  or  sensory  fasciculus  (occupying  the  external  third 
of  the  crusta),  Avliich  is  never  the  seat  of  secondary  degeneration. 
■  (2)  A  middle  fasciculus  (occupying  the  middle  third  of  the  crusta). 
which  is  the  usual  seat  of  secondary  degeneration. 

(3)  A  geniculate  fasciculus  (occupying  the  point  of  union  of  the 
middle  and  internal  thirds  of  the  crusta),  which  has  erroneously  been 
regarded  as  incapable  of  degeneration.  This  fesciculus  contains  fibres 
which  are  distributed  to  the  bulbar  centres,  and  are  concerned  in  the 
])rotluction  of  the  voluntary  movements  of  the  face  and  tongue. 


1-J(I        MOHBTl)    ANATOMY    OF    THE    NERVOUS    SYSTEM. 

(4)  An  (interior  fa^ekuhts  (occupying  the  internal  third  of  the 
cnistii),  degeneration  of  which  appears  only  to  be  associated  Avith 
intellectual  disorders. 

A  descending  degeneration  of  a  fcAv  of  the  fibres  of  the  superior 
peduncle  of  the  cei-ebclluni  has  been  observed.  In  a  case  reported  by 
Menilcl,  in  which  the  patient  had  suffered,  after  a  slight  apoplectic 
attack,  from  right-sided  hemiparesis  and  transitory  right-sided  henii- 
anivsthesia,  Avith  left-sided  heraiopia,  a  hemorrhagic  focus  about  the  size 
of  a  pea  Avas  found  in  the  pulvinar  of  the  left  optic  thalamus,  close  to 
tlic  internal  capsule.  Slight  evidences  of  descending  degeneration  of 
the  pyramidal  tract  on  both  sides  of  the  cord  Avere  found,  and,  in  addi- 
tion, a  streak  of  degeneration  was  followed  downwards  to  the  internal 
aspect  of  the  red  nucleus  of  the  same  side  ;  it  then  ascended  in  the 
tegmentum  and  crossed  over  to  the  superior  peduncle  of  the  cerebellum 
of  the  opposite  side,  and  was  followed  as  far  as  the  corpus  dentatum  of 
the  right  hemisphere  of  the  cerebellum  (Fig.  63). 

(c)    DKOENERATIONS    OF    NERVE    CENTRES    AND  CONDUCTING  PATHS  FROM    DISEASE. 

( j  )  Secondary  Degeneration  of  the  Spinal  Cord  after  Amputation. 

In  cases  of  long-standing  amputation  of  limbs,  the  posterior  roots  of 
the  nerves  are  found  slightly  diminished  in  size.  The  posterior  gray 
horn  on  that  side  is  also  relatively  diminished  in  size,  Avhile  some  of 
the  ganglion  cells  of  the  anterior  horns  completely  disappear,  and 
others  are  diminished  in  size  and  shorn  of  their  processes. 

( jj  )  Degeneration  of  Sensory  Ganglia  and  Conducting  Paths. 

The  facts  so  far  knoAvn  with  regard  to  degeneration  of  sensory  con- 
ducting paths  in  human  pathology  are  very  scanty.  Wlien  unilateral 
blindness  has  existed  for  a  long  time  the  optic  nerve  on  the  lilind  side 
has  been  found  atrophied,  but  the  tract  of  the  oi)posite  side  is  aifected 
to  a  greater  degree  than  that  of  the  same  side.  The  external  genicu- 
late l»ody  and  the  anterior  tubercle  of  the  corpora  quadrigemina  on  the 
side  oi)posite  the  blind  eye  have  also  been  found  smaller  than  the  corre- 
si)onding  i)arts  on  the  same  side.  Similar  phenomena  have  been  found 
by  Gudden  after  extirpation  of  one  eyeball  in  young  animals.  Tlie 
parieto-occipital  convolutions  of  the  left  hemisphere  of  the  brain  were 
extirpated  by  Gudden  in  a  young  dog,  and  he  afterwards  found  that 
the  external  geniculate  l)ody  and  the  optic  tract  of  the  same  side  were 
atrophied.  Experiments  of  this  kind  have  recently  been  cai-ried  out 
systematically  by  Monakow,  and  he  finds  that  extirpation  of  circum- 
scribed portions  of  the  cortex  is  followed  by  atrophy  of  strictly  defined 


DISSOLUTION    OF    THE    NERVOUS    SYSTEM.  121 

parts  of  the  optic  thalamus  and  adjoining  ganglia.  The  author  distin- 
guishes the  folloAving  areas  of  the  cortex :  (1)  Tlie  zone  of  the  rorpm 
geniculatum  externum,  so  named  because  extirjjation  of  it  caused  atrophy 
of  this  ganglion.  This  area  is  situated  in  the  posterior  superior  part 
of  the  hemisphere  ;  it  forms  about  one-third  of  the  hemisphere  and 
corresponds  to  Munk's  visual  sphere.  In  addition  to  the  external 
geniculate  body,  the  posterior  third  of  the  internal  capsule  with  the 
part  of  the  corona  radiata  which  lies  between  it  and  the  injured  cortex, 
the  lateral  layer  of  the  optic  thalamus,  the  stratum  zonale  in  part,  the 
optic  tract,  and  in  a  less  degree  the  tractus  peduuculus  transversalis, 
the  anterior  tubercle  of  the  corpora  quadi'igemina,  and  the  optic  nerves 
were  also  atr()[)hied.  (2)  The  zone  of  the  internal  genieulate  hody, 
which  is  situated  below  the  first  area  and  corresponds  to  Munk's  audi- 
tory sphere.  Extirpation  of  this  area  was  folloAved  Ijy  atrophy  of  the 
posterior  inferior  portion  of  the  internal  capsule,  along  with  the  portion 
of  the  corona  radiata  which  joins  the  atrophied  part  of  the  cajisule  with 
the  injured  portion  of  the  cortex,  and  in  a  less  degree  the  posterior 
part  of  the  stratum  reticulatum,  (3)  The  zone  of  the  lateral  nucleus 
of  the  optic  thalamus,  which  lies  in  front  of  the  first  zone  or  visual 
s})here.  Extirjiation  of  it  was  followed  by  atrophy  of  the  external 
nucleus  of  the  optic  thalamus,  the  outer  portion  of  the  crusta,  and  to  a 
less  extent  the  formatio  reticularis,  the  middle  peduncle  of  the  cere- 
bellum, and  the  corpus  trapezium.  (4)  The  zone  of  the  stratum  reti- 
culatiun  (Gitterschicht)  lies  to  the  outer  side  of  the  last  zone.  Extir- 
pation of  it  causes  atrophy  of  the  third  fifth  of  the  internal  capsule,  a 
part  of  the  lateral  portion  of  the  crusta,  the  anterior  part  of  the  stratum 
reticulatum,  and  to  a  less  degree  of  the  portion  of  the  tegmentum  Avhich 
lies  between  the  external  geniculate  body  and  the  posterior  tul;)ercle  of 
the  corpora  quadrigemina.  (5)  The  zone  of  the  anterior  tubercle  of 
the  optic  thalamus  is  situated  in  front  of  the  third  zone.  Extirpation 
of  it  causes  atroj)liy  of  the  anterior  tubercle  of  the  optic  thalamus,  the 
anterior  part  of  the  internal  capsule,  a  part  of  the  pyramidal  tract,  and 
to  a  less  degree  of  the  lamin;e  medullaris  of  the  anterior  tubercle, 
and  the  bundle  of  Vic(i(  d'Azyr.  (('))  The  zone  of  the  internal  nucleus 
of  the  optic  thalamus  occupies  the  anterior  area  of  the  cerebral  cortex. 
Extirpation  of  it  causes  atrojjhy  of  the  most  anterior  portion  of  the 
internal  capsule,  and  partial  atrophy  of  the  pyi-amidal  tract  aiul  the 
internal  nucleus  of  the  optic  thalamus.  (7)  External  to  the  zone  of 
the  anterior  tubercle  lies  another  zone,  extirpation  of  which  causes 
atrophy  of  the  anterior  portion  of  the  internal  caj)sule,  and  of  a  tract 
which  runs  direct  to  the  crus  cerebri,  which  is  suppose<l  by  Monakow 
to  contain  fibres  of  the  fjicial  and  hypoglossal  nerves. 


1:^-2        GEXEEAL    MOKHID    AXATOMY    AXD    PHYSIOLOGY. 

11.  GENERAL  MORBID  ANATOilY  AND  PHYSIOLOGY'. 

Tlie  i)i-ol>lem  of  morbid  physiology  is  to  interpret  morbid  functions 
by  morbid  .structures,  and  the  hiw  ^vhich  underlies  all  our  conclusions 
is  that  every  disordered  function  is  the  correlative  of  a  diseased  struc- 
ture :  and,  invensely,  that  every  diseased  structure  has  for  its  counter- 
pnrt  a  derangement  of  function.  It  may  be  laid  down  as  a  general 
law  that,  when  the  irritability  of  a  nervous  structure  is  increased,  it 
will  manifest  increased  functional  activity. 

It  may  be  supposed  that  a  free  arterial  sui)ply  to  a  part,  or  a  flushed 
condition  of  the  arterioles,  is  the  necessary  correlative  of  increased 
irritability  ;  and,  conversely,  that  a  diminished  arterial  supply,  with 
an  empty  and  contracted  condition  of  the  arterioles,  is  the  necessary 
correlative  of  diminished  irritability.  This  statement,  however,  can 
only  be  accepted  as  true  within  certain  limits  and  with  numerous  (piali- 
fications.  When  the  brain,  for  instance,  is  very  freely  supplied  with 
blood  so  that  its  substance  becomes  congested,  the  irritability  of  the  tis- 
sues is  no  doubt  at  first  increased.  It  must,  however,  be  remembered 
that  the  cranium  is  unyielding,  and  its  contents  practically  incompressi- 
ble, so  that  no  additional  (juantity  of  blood  can  enter  into  the  intra- 
cranial vessels  except  Ijy  displacing  a  corresponding  (piantity  of  some 
other  fluid.  When,  therefore,  the  vessels  become  dilated  beyond  certain 
nari-ow  limits  the  nervous  tissue  becomes  compressed,  the  material  e.x- 
changes  within  the  cranium  become  less  than  when  the  circulation  passes 
in  normal  (juantity  and  under  normal  pressure,  and  the  functional 
activity  of  the  organ  is  diminished  or  abolished.  A  similar  process  no 
doubt  occurs  in  the  spinal  cord  and  nerve  trunks.  Congestion  in  them, 
when  carried  beyond  certain  limits,  is  also  attended  with  diminution  of 
function,  due,  no  doubt,  to  compression  of  the  nerve  tissues  by  the 
dilated  vessels.  The  irritative  lesion  is  attended  with  increased  nutri- 
tive activity,  and  C()nse(iuently  with  free  arterial  supply  ;  but  this  lesion 
is  exceedingly  apt  to  terminate  in  the  opposite  condition  of  diminished 
nutrition  and  functional  activity.  The  first  stage  of  inflammation,  for 
instance,  is  an  irritative  lesion,  and  it  is  attended  by  excess  of  func- 
tional activity,  manifesting  itself  by  symptoms  of  hyperesthesia  and 
hyperkinesis ;  Init  when  the  nervous  tissues  become  partly  compressed 
by  effiised  pi-oducts  and  partly  disorganized  by  internal  changes,  the 
lesion  becomes  depressive,  and  the  symptoms  of  excess  give  place  to 
those  of  diminution  of  function;  in  other  words,  the  symptoms  of 
hyperaesthesia  and  hyperkinesis  give  place  to  those  of  anesthesia  and 
akinesis. 


GENERAL    MORBID    AXATOMY    AXD    PHYSIOLOGY.       123 

But  if  excess  of  nutrient  activity  is  not  always  accompanied  bv 
increased  functional  activity,  neither  is  diminished  nutrient  activity 
always  accompanied  by  diminution  of  functional  activity,  When  the 
nutrition  of  a  nerve  fibre  is  gradually  lessened  its  irritability  becomes, 
indeed,  increased  instead  of  diminished.  The  stock  of  irritable  matter 
which  the  nerve  fibre  possesses  is  no  doubt  less  under  these  circum- 
stances, but  an  increased  readiness  to  discharge  the  energv  is  mani- 
fested  :  and  it  is  notorious  that  feeble  and  angemic  persons  manifest  an 
undue  readiness  to  respond  to  the  action  of  stimuli  of  all  kinds,  a 
condition  which  is  correctly  designated  nervous  irritahUity.  One  other 
important  consideration  must  be  taken  into  account  before  the  amount 
of  nourishment  supplied  to  an  organ  or  a  tissue  can  be  accepted  as  in 
any  way  a  measure  of  the  functional  activity  of  the  latter.  When  a 
strong  faradic  current  is  sent  through  the  sciatic  nerve  of  a  frog,  the 
gastrocnemius  muscle  contracts  strongly ;  but  a  subsequent  current 
])assed  through  the  nerve  is  followed  by  no  reaction  until  the  irritability 
of  the  nerve  is  restored  by  the  absorption  of  more  nourishment.  A 
similar  process  doubtless  occurs  in  disease  of  the  nervous  system. 
\yhen  a  part  is  supplied  with  an  excessive  amount  of  nourishment,  the 
tissues  become  so  irritable  that  they  discharge  readily,  either  sponta- 
neously, or  in  response  to  stimuli  which  would  not  affect  them  under 
normal  conditions.  Under  these  circumstances,  excessive  discharges  of 
nervous  energy  readily  take  place,  and  these  are  followed  by  temporary 
loss  of  irritability,  and  the  tissue  becomes  incapable  for  a  time  of  per- 
forming its  normal  functions.  The  excessive  liberations  of  energy 
from  the  cortex  of  the  brain,  which  occasion  epileptic  attacks,  for 
instance,  are  accompanied  by  loss  of  consciousness,  which  lasts  for  a 
considerable  time,  and  the  convulsive  phenomena  are  not  unfrequently 
followed  by  temporary  motor  paralysis.  When  the  energy  of  the 
dischargbui  lesion  is  once  liberated,  the  part  affected  becomes  incapable 
of  performing  its  functions,  until  its  irritability  is  restored  by  the 
absorption  of  a  fresh  stock  of  irritable  matter.  The  primary  effect  of 
almost  all  chemical  agents  on  the  nervous  system  is  to  stimulate  it,  and 
to  increase  its  functional  activity,  Avhile  their  secondary  effect  is  to 
depress  or  abolish  its  functional  activity.  The  stimulant  action  of 
alcohol  on  the  brain,  for  instance,  is  followed  by  a  stage  of  depression, 
which  may  amount  to  complete  abolition  of  the  cerebral  functions  or 
coma.  Strychnine  increases  the  irritability  of  the  gray  substance  of 
the  spinal  cord ;  but  the  reflex  actions,  which  are  at  first  greatly  exag- 
gerated, become  ultimately  abolished,  and  the  animal  poisoned  by 
strychnine  often  dies  from  paralysis.  Curara,  which  may  be  taken  as 
the  type  of  nervous  sedatives,  paralyzes  the  terminations  of  the  motor 


124      GENERAL    MORBID    ANATOMY    AND    PHYSIOLOPxY. 

nerves,  yet  Bernard  i)rove(l  that  it  first  increases  the  irritability  of  the 

fibres. 

Tlie  direct  tendency  of  all  destroying  lesions  is  to  abolish  function. 
It  111  list,  however,  be  remembered  that  these  lesions  are  frequently  sur- 
rounded by  a  zone  of  nervous  tissue  Avhich  is  in  a  state  of  irritation, 
and  the  prominent  symptoms  of  the  affection  are  often  produced  by  tliis 
zone,  consequently  the  symptoms  may  be  indicative  of  excess  of  func- 
tional activity.  A  gummatous  tumor,  for  instance,  in  the  cortex  of  the 
brain  is  generally  declared  by  epileptoid  convulsions ;  yet  the  direct 
tendency  of  the  tumor,  in  so  far  as  it  has  destroyed  and  replaced  ner- 
vous tissue,  is  to  abolish  function.  In  such  cases,  both  the  direct  and 
indirect  effects  of  the  tumor  are  often  manifested :  the  former  by  para- 
lytic and  the  latter  by  convulsive  symptoms.  Even  the  ischa?mic  soften- 
ing, caused  by  plugging  of  vessels,  is  often  surrounded  by  a  congestive 
zone  of  tissue,  and  the  latter  may  give  rise  to  symptoms  of  irritation. 


CHAPTER  lY. 

GENERAL  SYMPTOMATOLOGY. 

Disease  of  the  nervous  system  gives  rise  to  disorders  (A)  in  the 
feelings  of  the  patient — the  a'sthesio7ieuroses,  (B)  in  the  nutrition  of 
the  various  tissues  of  the  body — the  trojjJwneuroses,  and  (0)  in  the 
movements  of  the   body    as    a  Avhole    and  of  its    various    parts — the 

kinesioneui'oses. 

A.  THE  .ESTHESIONEUllOSES. 

The  assthesioneuroses  may  be  divided  into  disorders  (i)  of  the  primary 
or  elementary  feelings — the  prima)'!/  ajsthesioneuroses,  and  (ii)  of  the 
secondare/  or  compound  feelings — the  secondary  nesthesioneuroses,  while 
each  of  these  divisions  may  be  subdivided  into  (1)  disorders  of  the 
common  subjective  or  emotional  feelings  (pleasures  and  pains),  and  (2) 
the  s})ecial.  objective,  or  intellectual  sensations. 

1.    TjIE    PkI.M.VUY    .ESTIIESIOXEUROSES. 

The  general  disorders  of  the  feelings  consist,  first,  of  excess  of  the 
normal  sensation  caused  by  a  stimulus,  which  is  named  hypera'sthesia 
when  the  objective  feelings  are  increased  in  acuteness,  and  hypcrahiesia 
when  the  common  sensation  of  pain  is  increased ;  secondly,  of  diminu- 
tion of  the  normal  sensation  evoked  by  a  stimulus,  which  is  named 
awcsthesia  when  the  objective  feelings  are  diminished,  and  analgesia 
when  the  subjective  feelings  are  diminished  in  acuteness :  tJiirdly,  of 
l)aroxysms  of  pain  in  the  region  of  distribution  of  a  sensory  nerve  in 
the  absence  of  external  stimulus  or  active  inflammation  of  the  nerve, 
named  neurcdgia ;  fourtldy,  of  abnormal  sensations,  such  as  )iunil)ness, 
tickling,  crawling,  itching,  and  feelings  of  heat  and  cold,  also  felt  in 
the  absence  of  external  stimulus,  and  grouj^ed  togetlier  under  the  name 
of  parcesthesiCB  ;  and  fifthly,  a  diminution  or  increase  of  the  interval 
wliich  elapses  between  the  instant  at  which  a  stimulus  is  applied  to  a 
sensory  surface  and  the  moment  at  wliich  the  suliject  makes  a  voluntary 
effort  to  indicate  that  the  sensation  has  l)een  perceived,  named  accelera- 
tion or  retardation  of  sensory  perception  respectively. 

Disorders  of   the   primary  or   elementary  feelings    may  be  divided 


y2i]  GENERAL    SYMPTOMATOLOGY. 

■iccordin- to  the  tissues  and  organs  implicated  into  sensory  afiections : 
1  of  the"  skin  and  exposed  parts  of  the  mucous  meml.ranes  :  2.  the 
voluntary  muscles;  3,  the  bones  and  joints;  4,  the  viscera;  5,  the 
special  senses.  The  anatomical  division  is  traversed  at  right  angles  by 
a  physiological  division  into  sensory  disorders  of  (1). the  common  or 
subjective  feelings,  and  (2)  the  special  or  objective  feelings. 


1.  Cutaneous  ^Esthesioneuroses. 

Sensory  disorders  are  known  through  the  statements  and  gestures  of 
the  patient,  and  the  information  obtained  by  this  means  must  be 
checked  by  a  systematic  examination. 

The  foilowino-  tests  of  the  various  forms  of  cutaneous  sensory  dis- 
orders may  be  used  at  the  bedside  : 

[a)  Common  cutaneous  sensations  may  be  tested  by  the  i»rick  of  a 
pin,  application  of  heat  and  cold,  i)inching,  and  firm  pressure,  or  the 
application  of  the  faradic  current. 

(7;)  The  rapidity  of  sensory  conduction  may  be  tested  by  getting  the 
patient,  with  closed  eyes,  to  give  a  signal  by  voice  or  by  a  tap  on  a 
table  immediately  on  feeling  the  prick  of  a  pin,  and  noting  the  interval 
which  elapses  between  the  prick  and  the  signal. 

(c)  The  sense  of  pressure  may  be  tested  by  Weber's  method,  which 
consists  of  the  superimposition  of  weights  to  determine  the  smallest 
difference  which  can  be  perceived.  To  exclude  the  muscular  sense  the 
part  to  be  tested  should  be  at  rest  on  a  table,  and  the  sensation  of  tem- 
perature may  be  excluded  by  the  interposition  of  a  bad  conductor  like 
a  wooden  disk. 

(d)  The  sense  of  locality  may  be  tested  by  touching  some  part  of  the 
surface  with  the  finger  or  point  of  a  needle  whilst  the  j)atient"s  eyes 
are  closed,  and  asking  him  to  indicate  the  point  touched.  A  better 
plan  is  to  ascertain  to  what  distance  the  points  of  a  compass  must  be 
separated  from  one  another  before  they  are  felt  as  two.  The  distance 
to  which  the  points  of  the  compass  must  be  separated  varies  for  differ- 
ent regions  of  the  body,  so  that  the  observer  must  know  the  normal 
scale  of  difference  before  drawing  any  conclusions  from  the  results 
obtained,  but  in  many  cases  valuable  information  may  be  obtained  by 
comparing  the  anaesthetic  area  with  the  corresponding  part  on  the 
opposite  side,  which  may  be  normal. 

{e)  The  sense  of  temperature  is  tested  by  applying  hot  and  cold 
bodies  to  the  surface  when  the  patient's  eyes  are  closed,  and  asking 
him  to  indicate  each  time  whether  the  temperature  of  the  touching 
body  was  hot  or  cold.     Two  test-tubes,  one   filled  with   cold   aii.l   the 


THE    PEIMARY    .ESTHESIOXEUROSES.  127 

Other  with  hot  water,  aiiSAver  the  purpose  of  testing  very  well,  or  two 
silver  spoons,  one  clipped  in  hot  and  the  other  in  cold  water,  are 
e([ually  efficient  and  often  more  convenient. 

(/)  'i'lie  sense  of  touch  is  a  compound  sensation,  but  it  may  be 
roughly  tested  by  means  of  a  light  touch  with  a  featlier,  and  asking 
the  patient  to  indicate  with  closed  eyes  each  time  he  is  touched. 

a.  Cutaneous  Hyper.esthesi.e. 

(1)  Hyperpselaphesia,  or  abnormal  acuteness  of  tactile  sensibility, 
declares  itself  by  excessive  reaction  to  the  various  tests  for  the  senses 
of  pressure  and  locality.  A  smaller  difference  than  usual  in  the  in- 
crease of  pressure  is  perceptible,  and  the  diameters  of  the  areas  of 
sensibility  are  unusually  small. 

(2)  Foli/ccsthesia  is  the  condition  in  which  one  point  of  the  compass 
on  being  placed  on  the  skin  is  felt  as  two,  three,  or  five  points. 

(3)  AllocJdria  is  a  condition  in  Avliich  the  patient  is  not  sure,  and  is 
often  in  error  when  the  eyes  are  closed,  as  to  w^hich  side  of  the  bodv  is 
touched,  even  though  the  cutaneous  sensibility  is  more  or  less  normal 
in  other  respects. 

(4)  Girdle  seiisations  consist  of  a  subjective  perception  Avhich  pro- 
duces the  impression  of  having  a  girdle  or  a  broad  bandage  tied  about 
the  trunk  or  limbs. 

(o)  TJierj7io-Jti/pe)restJiesia  consists  of  an  alniormal  acuteness  of  the 
sense  of  temperature,  so  that  differences  in  temperature  so  slight  as  to 
be  inappreciable  in  health  are  recognized. 

(0)  Causalgid  is  a  name  given  by  Dr.  S.  Weir  Mitchell  to  a  distress- 
ing pain  which  appears  to  belong  to  the  thermo-hypersesthesiee.  It  is 
described  by  patients  as  an  intensely  burning  sensation,  and  is  compared 
to  that  caused  by  a  mustard  plaster,  or  by  ''  a  red-hot  file  rasping  the 
skin.'"  It  is  generally  associated  with  "  glossy  skin,"'  but  often  pre- 
cedes the  trophic  changes  of  the  skin. 

(7)  Dy^cesthnia  is  a  term  introduced  by  Charcot  to  indicate  a  sensa- 
tion of  a  peculiarly  distressing  and  vibratory  character,  which  ascends 
towards  the  central  end  of  a  limb  and  descends  towards  its  extremity. 
The  sensation  is  excited  by  the  slightest  touch  or  the  application  of  a 
cold  body  to  the  surface,  and  it  persists  from  several  minutes  to  a 
quarter  of  an  hour  after  the  exciting  cause  has  ceased  to  act.  After  a 
short  time  an  analogous  sensation  may  be  felt  at  a  corresponding  point 
of  the  limb,  opposite  to  the  one  primarily  excited. 

(8)  Hyperce-'sthetie  spots  consist  of  circumscribed  patches  of  skin 
which  are  exquisitely  painful  to  touch,  and  which  are  subject  to  attacks 
of  spontaneous  pains  of  a  burning  character. 


l-)s  genp:ral  symptomatology. 

(!))  Cutaneous  hyperalgesia  consists  of  an  increased  sensibility  of 
the  common  sensations,  and  is  much  more  frequent  tlian  increase  of 
tactile  sensibility.  In  this  condition,  stimuli,  Avhich  in  health  give  rise 
to  touch,  or  even  to  pleasant  sensations  like  the  minor  degrees  of  tick- 
liiiii-.  noAV  become  i)ainful.  Thermo-hjperahjesia  may  be  applied  to 
desiijnate  the  condition  in  which  contact  Avith  a  hot  or  cold  body  gives 
risernot  to  a  feeling  of  temperature,  but  to  a  i)ainful  sensation. 

I).  Cutaneous  An^esthesi.e. 

(1)  Distribution  of  Ancesthesia. — Anaesthesia  or  sensory  paralysis  is 
sometimes  distributed  in  limited  patches  or  in  the  area  of  distribution 
of  particular  nerves,  and  it  is  then  termed  cirrumscriht'd  anaesthesia. 
At  other  times  it  appears  in  the  form  of  a  zone  of  variable  Avidth  sur- 
rounding the  bodv  on  one  or  both  sides,  and  it  is  then  named  anaesthesia 
in  the  form  of  a  girdle.  When  it  is  distributed  over  the  lower  half  of 
the  body  and  the  lower  extremities  it  is  tei'med  parana'sthesia ;  and 
when  over  the  lateral  half  of  the  body,  including  half  tlie  face  and  the 
extremities,  it  is  named  heiiiiana'sthesia. 

(2)  Total  anaesthemi  is  a  diminution  or  loss  of  every  form  of  cuta- 
neous sensibility,  and  partial  anaesthesia  a  diminution  or  loss  of  certain 
forms  of  sensibility  while  others  are  preserved. 

(8)  Api^elapliesia  or  tactile  ancesthesia  denotes  a  diminution  or  h)ss 
of  the  acuteness  of  tactile  sensibility,  a  condition  which  is  fre([uently 
associated  with  hyperalgesia.  Severe  pain  is  sometimes  felt  in  anes- 
thetic parts,  and  the  condition  is  then  called  anaesthesia  dolorosa. 

(4)  Thermo-ana'Sthesia  means  insensibility  to  heat  or  cold,  a  condi- 
tion which  sometimes  occurs  as  an  isolated  affection. 

("))  Analgesia  diQiioie^  a  diminution  or  loss  of  the  sensation  of  i»ain. 
Analgesia,  with  preservation  of  the  tactile  sensibility,  is  the  most  fre- 
(pient  form  of  partial  sensory  paralysis. 

(6)  Retardation  vf  sensory  conduction  may  be  employed  as  a  test  of 
any  form  of  auBesthesia,  and  gives  rise  in  the  partial  varieties  to  the 
following  anomalous  phenomena  : 

(a)  Separation  of  Tactile  and  Painful  Impressions. — In  locomotor 
ataxia  the  prick  of  a  needle  causes  a  prompt  feeling  of  touch,  which  is 
often  followed  in  two  or  three  seconds  by  a  feeling  of  pain.  In  cases 
of  thermo-ansesthesia,  a  test-tube  holding  hot  water  may  at  first  give 
rise  to  an  immediate  feeling  of  touch,  to  be  followed  in  two  or  three 
seconds  by  a  sensation  of  temi»erature. 

(h)  Double  Painful  Sensations.— In  some  cases  of  locomotor  ataxia, 
pricking  the  skin  on  the  back  of  the  foot  with  a  needle  is   sometimes 


THE    PRIMARY    .ESTHESIONEUROSES .  129 

followed  bv  a  first  painful  sensation,  and,  when  this  subsides,  bv  a 
sec(»nd  painful  sensation,  which  is  usually  of  greater  intensity  and  more 
prolonged  than  the  first.  The  first  is  felt  after  a  lapse  of  two  and  a 
half  to  three  seconds  subsequent  to  the  prick,  but  the  second  is  not 
felt  until  after  another  interval  of  from  two  to  five  seconds. 

{(■)  Persistent  After-sensations. — In  some  cases  of  partial  ansesthesia, 
pinching  the  skin  or  pricking  with  a  needle  gives  rise  to  a  sensation 
which  begins  slowly,  but  gradually  increases  in  intensity,  and  is  much 
more  severe  than  the  i)ain  which  occurs  in  health. 

{d)  Inability  to  Count  Successive  Impressions. — Closely  connected 
with  these  persistent  afiter-sensations  is  the  inability  of  the  patient  to 
count  correctly  several  imi)res.sions  made  in  quick  succession.  Enume- 
ration of  successive  impressions  presupposes  an  interval  to  elapse 
between  the  sensation  caused  by  each ;  but,  when  the  conduction  is 
retarded,  each  sensation  is  unusually  prolonged  so  that  the  first  does  not 
fade  before  the  second  begins,  and  so  counting  Ijecomes  impossible. 

c.  Cutaneous  Par.esthesi.e  and  Paralgesia. 

(1)  Pruritus  is  a  sensation  caused  l)y  aluiormal  irritation  of  the 
nerve-ends  of  the  papillae  of  the  skin,  or  by  a  state  of  undue  irrita- 
bility of  these  nerve  terminations  themselves.  Pruritus  is  related  to 
such  sensations  as  tickling  and  to  burning  and  stinging  pains,  but  an 
irresistible  tendency  to  scratch  is  its  characteristic  symptom. 

('2)  Formication  does  not  amount  to  pain,  but  is  described  as  a  feel- 
ing of  creeping  or  pricking,  or  is  compared  to  the  crawling  of  ants. 
Formication  occurs  as  a  transitory  symptom  in  minor  mechanical  in- 
juries of  nerve-trunks,  and  is  felt  in  the  foot  as  a  sensation  of  "  pins 
and  needles,"  numbness,  or  ''sleepy  sensation,"  Avhen  the  sciatic  nerve 
is  compressed  for  some  time. 

d.  Neuralgia  and  Neuralgiform  Pains. 

(1)  Neuralgia  consists  of  periodic  attacks  of  severe  pain,  occurring 
suddenly  and  spontaneously  in  the  course  of  one  of  the  larger  nerve- 
trunks,  and  ramifying  in  a  few  or  all  of  its  sensory  branches. 

The  character  of  the  pain  in  cutaneous  neuralgia  will  be  described 
when  the  special  forms  of  it  are  under  consideration,  but  we  shall  here 
refer  to  some  of  the  more  prominent  phenomena  of  the  affection. 
During  the  height  of  the  neuralgic  paroxysm  there  is  an  irradiation 
of  the  jMin  to  other  sensory  nerves,  generally  to  branches  of  the  same 
trunk  or  to  neighboring  nerves,  but  occasionally  to  more  or  less  distant 
nerves,  and  the  neuralgic  pain  is  accompanied  by  various  parsesthesiae, 
hyperaesthesia,  or  sometimes  anaesthesia. 

0 


130  GENERAL    SYMPTOMATOLOGY. 

Painful  Points.— These  points  were  first  described  by  Yalleix  under 
the  name  of  jyoints  douloureux.  An  examination  of  the  part  during 
an  attack  of  superficial  neuralgia  will  reveal  one  or  more  points  which 
are  extremely  sensitive  to  the  pressure  of  the  tip  of  the  finger.  The 
sensitiveness  of  these  points  stands  almost  in  a  direct  relation  with  the 
severity  of  the  paroxysms,  but  they  may  be  present  occasionally  during 
the  period  of  remission,  and  in  some  cases  pressure  upon  them  induces 
an  attack.  These  tender  spots  are  found  at  various  points  in  the 
course  of  the  affected  nerves,  when  their  trunks  pass  from  a  deeper  to 
a  more  superficial  level,  and  especially  where  they  emerge  from  bony 
canals  or  pierce  fibrous  fascia?,  or  even  where  a  nerve  lies  on  a  hard 
bed  so  that  it  may  be  easily  compressed. 

Point  Apophymire. — Trousseau  believed  that  in  all  forms  of  neural- 
gia the  spinous  processes  of  the  vertebrae  corresponding  to  the  origin 
of  the  painful  nerve,  and  which  he  calls  points  apophysaire  or  spinous 
points,  are  painful  on  pressure,  but  these  points  are  also  present  in 
spinal  irritation  and  in  myalgia.  The  concomitant  symptoms  of 
neuralgia  will  be  described  along  with  the  special  forms  of  neuralgia. 

(2)  Lightning-like  Pains. — In  locomotor  ataxia  patients  often  suffer 
from  spontaneously  occurring  paroxysms  of  distressing  pains,  which 
are  compared  by  them  to  forked  lightning  darting  through  the  body, 
and  have  been  described  under  the  name  of  general  neuralgia,  or 
neuralgic  rheumatism. 

2.  Sensory  Affections  of  the  Voluntary  Muscles 
{^Muscular  ^-Esthesioneuroses) . 

a.  Muscular  Hyper^esthesia  and  Hypkralgesia. 

The  feeling  of  unrest  and  desire  for  constant  change  of  position, 
called  the  ''fidgets,"'  appears  to  be  due  to  muscular  hypene^thesla.  In 
spasmodic  wry-neck,  and  in  "cramps"  the  hyperiesthetic  condition  is 
often  very  great,  and  causes  intense  pain.  The  excessive  feeling  of 
fatigue  and  prostration  which  occurs  on  slight  exertion  in  the  prodromal 
stage  of  acute  diseases,  is  probably  due  to  an  increasing  muscular  sen- 
sibility, and  consequently  this  condition  may  be  regarded  as  a  muscular 
hyperalgesia.  Painful  conditions  of  the  muscles  are  called  myalgia  or 
myodynia.  Pain  is  most  frequently  met  with  in  the  muscles  of  the 
neck  and  of  the  lumbar  region,  and  inasmuch  as  it  corresponds  to 
cutaneous  neuralgia  and  arthralgia,  it  may  be  called  muscular  neuralgia 
or  myoneuralgia. 


THE    PRIMARY    .ESTHESIONEUROSES.  131 

h.  Muscular  Ax^sthesia. 

Muscular  aniiestliesia  consists  of  diminution  or  loss  of  the  common 
sensibility  and  of  the  sense  of  muscular  effort.  When  muscular  sensi- 
bility is  lost,  as  tested  by  the  faradic  current,  while  the  muscular  sense 
is  retained,  the  condition  is  termed  muscular  analgia,  or  muscular 
analf/rsi((.  When  there  is  a  diminution  or  loss  of  the  capacity  of  rec- 
ognizing small  weights,  or  of  perceiving  small  differences  by  means  of 
muscular  effort  with  closed  eyes,  the  condition  is  called  ancesthesia  of 
the  muscular  sense. 

(1)  Tests  of  Muscular  Sensibility. — The  state  of  muscular  sensi- 
bility is  best  tested  by  the  faradic  current.  When  a  healthy  muscle  is 
made  to  act,  a  dull  feeling  accompanies  the  contraction,  this  feelino- 
being  much  increased  in  muscular  hyperalgesia  and  diminished  or  lost 
in  muscular  analgesia. 

(2)  Tests  for  Muscular  Sense. — To  test  the  muscular  sense  the 
patient  should  be  made  to  lift  various  weights,  and  to  form  an  estimate, 
with  closed  eyes,  of  the  weights  and  of  the  differences  of  successive 
Aveights.  In  order  to  eliminate  the  cutaneous  sense  of  pressure,  the 
weights  should  be  placed  in  a  cloth  and  suspended  from  the  limb  to  be 
tested.  The  patient  may  also  be  made  to  move  the  limb  into  certain 
prescribed  positions,  with  closed  eyes ;  he  may  be  asked  to  touch  a 
particular  part  of  the  body,  such  as  the  tip  of  the  nose,  with  the  index 
finger,  to  take  hold  of  a  ticking  watch  held  before  him,  or  to  describe 
an  imaginary  circle  on  the  floor  with  the  big  toe.  The  patient  fails  to 
accomplish  these  actions  with  precision  when  there  is  muscular 
ancesthesia. 

8.  Sensory  Affections  of  the  Joints  and  Bones 
{Articular  and  Osseous  jEsthesioneuroses). 

a.  Osteoneuralgia. 

The  bones  are  sometimes  the  seat  of  severe  pain,  and  when  the  pain 
is  not  caused  by  recognizable  anatomical  changes  the  condition  is  re- 
garded as  a  neuralgia,  and  named  osteoneuralgia. 

Neuralgia  of  the  bones  differs  from  cutaneous  neuralgia  in  not  radiat- 
ing along  the  course  of  the  principal  Ijranches  of  the  affected  nerves. 
It  is  probable  that  the  sensory  nerves  of  the  Ijones  reach  them  along 
with  the  sympathetic  plexus  which  surrounds  the  vessels. 


2^32  GENERAL    SYMPTOMATOLOGY. 

6.  Arthroneuralgia. 

Arthroneuralgia  consists  of  severe  neuralgiform  pains  in  a  joint  in 
the  absence  of  any  recognizable  anatomical  alteration  of  it.  The  pain 
occurs  in  paroxysms  which  come  on  spontaneously,  and  which  are  sep- 
arated by  intervals  of  complete  or  comparative  freedom  from  pain. 
The  pain  is  sometimes  described  as  tearing,  or  shooting  through  the 
joint  like  lightning,  and  at  other  times  as  a  boring  or  stabbing  pain. 

The  patient  may  also  complain  of  numbness  and  formication  about 
the  joint,  or  of  sensations  of  heat  and  cold,  and  the  skin  over  the  joint 
is  often  hyperjesthetic  in  the  early  stages  of  the  affection,  and  anaes- 
thetic when  it  is  of  long  standing.  The  pain  is  much  increased  when 
tlie  patient's  attention  is  directed  to  it,  while  it  is  diminished  under  the 
influence  of  general  fatigue,  and  does  not  prevent  the  patient  from 
sleeping.  Pressure  increases  the  pain,  but,  as  occurs  in  cutaneous 
neuralgia,  slight  and  superficial  pressure  may  produce  intense  pain, 
while  deep,  continuous,  and  uniform  compression  produces  no  effect,  or 
even  relieves  the  pain.  Painful  points  may  be  obtained  on  pressure, 
but  their  position  is  somewhat  indefinite.  Neighboring  nerve-trunks 
may  also  be  found  painful  on  pressure,  and  the  spines  of  some  of  the 
vertebra  may  likewise  be  tender  to  pressure.  In  some  cases  spastic 
contraction  of  the  muscles  surrounding  the  joint  occurs,  while  in  other 
cases  the  limb  is  feeble  and  lie]i)less,  owing,  perhaps,  to  the  fear  of 
inducing  a  paroxysm  of  pain  by  movement  at  the  joint  rather  than  to 
any  muscular  paralysis. 

The  vaso-motor  disturbances  consist  of  redness,  heat,  and  increased 
secretion  of  sweat  in  the  neighborhood  of  the  affected  joint,  and  a  cir- 
cumscribed dough  or  fluctuating  swelling  is  sometimes  observed  in  the 
skin  over  the  joint,  which  was  compared  by  Brodie  to  an  unusually 
large  urticaria  wheal.  Swelling  of  the  joint  from  serous  effusion  within 
the  capsule  may  occasionally  take  place,  and  is  apt  to  be  regarded  as  of 
inflammatory  origin,  and  when  effusion  takes  place  in  the  tissues  sur- 
rounding the  joint  as  the  result  of  irritating  applications,  the  diagnosis 
is  still  further  obscured. 

4.    Sensory  Affections  of  the  Internal  Organs 
( Visceral  ^sthesionniroses). 

The  visceral  sensations  belong  to  the  common  or  subjective  sensa- 
tions, and  consequently  excess  of  a  normal  visceral  feeling  may  be 
regarded  as  a  hyperalgesia,  while  an  altogetlier  abnormal  visceral  feel- 
ing belongs  to  the  parmsthesim ;  but  it  is  by  no  means  easy  to  draw  a 
distinction  between  these  two  kinds.     Diminution  or  loss  of  the  visceral 


THE    PRIMARY    .ESTHESIOXEUROSES .  133 

feelings  constitutes  a  visceral  ancesthcsia,  or,  more  correctly,  a  visceral 

a.  Visceral  Hyperalgesi.e  and  Paralgesia. 

(1)  Titillation  is  a  sensation  induced  by  irritation  of  the  sensory 
brandies  of  the  vagus,  especially  the  superior  laryngeal  branch,  or  by 
undue  irritability  of  the  ends  of  the  nerve,  and  corresponds  with  pru- 
ritus of  the  external  skin ;  and  as  pruritus  leads  to  an  irresistible  ten- 
dency to  scratching,  so  titillation  leads  to  the  reflex  respiratory  move- 
ments Avhich  produce  coughing. 

(2)  G-Iobus  is  a  sensation  which  gives  the  feeling  of  a  ball  ascending 
from  the  epigastric  region  to  the  throat.  It  is  a  frequent  symptom  of 
hysteria,  and  occasionally  forms  the  aura  of  an  epileptic  attack.  Globus 
is  supposed  by  some  to  be  caused  by  spasm  of  the  oesophagus  and 
pharynx,  and  it  has  consequently  been  called  oesophagismus,  but  the 
explanation  is  not  a  satisfactory  one. 

(3)  Pyrosis  or  water-brash  is  a  painful  sensation  in  the  epigastrium, 
consisting  of  a  sense  of  burning,  which  is  generally  attended  with  the 
rising  of  a  ((uantity  of  clear  watery  and  strongly  alkaline  fluid  into  the 
mouth.  An  attack  of  pyrosis  may  last  from  a  few  minutes  to  many 
hours,  with  alternating  remissions  and  exacerbations,  and  is  most  prob- 
ably caused  by  a  spasm  of  the  cardiac  end  of  the  stomach  when  its 
contents  are  very  acid,  thus  arresting  the  secretion  of  saliva  in  the 
oesophagus. 

(4)  Bulimia  is  a  feeling  of  hunger,  which  is  abnormal  in  its  period 
of  occurrence  or  in  its  intensity,  and  which  is  appeased  only  for  a  short 
time  by  taking  food. 

(5)  Polydipsia  is  an  excessive  feeling  of  thirst,  and  is  a  constant 
symptom  of  polyuria  and  diabetes,  and  is  an  occasional  symptom  in 
hysteria. 

(6)  Excessive  voluptuous  feelings  arise  without  any  exciting  cause  in 
both  sexes,  and  are  associated  with  the  erections  and  ejaculations  which 
accompany  normal  coitus.  These  sensations  may  be  caused  by  a  local 
irritation  of  the  genitals,  or  by  a  central  disease  like  tabes  dorsalis. 

(7)  Feeling  of  oppt'ession  arises,  when  general,  from  overwork  or 
deficient  nourishment  of  the  nervous  system.  It  is  described  by  the 
patient  as  a  feeling  of  heaviness,  dulness,  and  depression  of  spirits.  A 
more  specific  form  of  oppression  occurs  in  connection  with  cardiac 
aff'ections,  which  will  be  subsequently  described  as  angina  pectoris. 

b.  Visceral  Anaesthesia  and  Analgesia. 
Very  little   is  known  with   regard  to   diminution  or  loss  of  visceral 
feeling.     The  normal  functions  of  the  viscera  are  performed  without 


134  GENERAL    SYMPTOMATOLOGY. 

definite  sensibility,  although  a  diffused  visceral  sensibility  contributes 
greatly  to  our  feeling  of  comfort  and  well-being,  and  it  is  probable  that 
diminution  of  visceral  sensations  contributes  in  a  corresponding  degree 
to  our  o-eneral  feeling  of  bodily  discomfort.  Visceral  anaesthesia  is  best 
defined'^in  the  organs  which  are  most  in  relation  with  external  forces, 
such  as  the  larynx,  stomach,  sexual  organs,  and  rectum. 

(1)  Ancestliesia  of  the  laryngeal  and  bronchial  branches  of  the  vagus 
renders  titillation  and  the  consequent  reflex  act  of  coughing  impossible. 
In  this  condition  catarrhal  secretions  fail  to  be  expelled,  and  may  by 
their  accumulation  cause  suffocation. 

(2)  Ancesthrsia  in  the  territorg  of  the  gastric  branches  of  the  vagus 
gives  vise  to  polgj^hagia,  &  condition  in  which  an  unusual  quantity  of 
food  must  be  taken  before  the  feeling  of  hunger  is  appeased,  or  in  which 
the  feeling  of  repletion  is  never  obtained  however  much  food  is  taken. 
The  experiments  of  Brachet,  Arnold,  and  others  have  proved  that,  on 
section  of  the  vagi,  animals  continue  to  eat  until  the  oesophagus  is 
filled  with  food. 

(3)  Ancesthesia  of  the  sexual  feelings  is  most  frequently  observed  in 
the  female  sex.  Complete  absence  of  voluptuous  feelings  in  hysterical 
females,  along  with  diffused  or  circumscribed  cutaneous  angesthesia,  is 
most  probably  due  to  anaesthesia  of  the  mucous  membrane  of  the 
vagina.  Anaesthesia  of  the  genitals  is  observed  in  the  male  sex  as  a 
result  of  sexual  excesses  or  onanism,  or  as  a  symptom  of  chronic  affec- 
tions of  the  spinal  cord,  such  as  spinal  meningitis  and  tabes  dorsalis, 
or  in  the  absence  of  any  appreciable  cause.  In  such  cases  the  electrical 
sensibility  of  the  glans  penis  and  of  the  external  genitals  is  diminished, 
and  the  power  of  erection  is  lost,  constituting  impotency ;  or  the  loss  of 
reflex  irritability  arrests  the  secretion  of  semen  and  abolishes  the  power 
of  ejaculation,  a  condition  named  asperinatisin. 

(4)  Ancesthesia  of  the  mucous  membrane  of  the  rectum,  which  is  a 
frequent  symptom  of  grave  organic  diseases  of  the  spinal  cord,  permits 
the  stools  to  pass  unconsciouslv. 

(5)  Ancesthesia  of  the  mucous  membrane  is  probably  present  in  the 
early  stages  of  many  cases  of  locomotor  ataxia,  and  causes  great  toler- 
ance of  the  bladder  to  its  contents.  The  bladder  may  become  greatly 
distended  without  giving  rise  to  the  desire  to  micturate.  Anaesthesia 
of  the  mucous  membrane  of  the  urethra  produces  a  condition  in  which 
the  urine  may  pass  in  a  full  stream  without  the  knowledge  of  the  patient. 

5.  Sensory  Disorders  of  the  Special  Senses. 

The  consideration  of  this  part  of  the  aesthesioneuroses  is  reserved  for 
special  mention  in  a  later  part  of  this  work. 


SECONDARY    OR    COMPOUXI)    J^STHESIOXEUROSES .      135 


II.  The  Secondary  or  Compound  ^Esthesioneuroses. 

The  sensory  conducting  paths  unite  with  each  other  for  the  first  time 
on  reaching  the  common  centre  of  sensory  connections — the  scnsorium 
commune;  and  molecular  change  in  this  centre  is  the  correlative  of 
the  compound  feelings  and  cognitions,  while  an  abnormal  molecular 
discharge  from  this  centre  is  the  correlative  of  the  disorders  of  the 
compound  feelings  comprised  under  the  name  of  the  secondary  aesthesio- 
neuroses.  But  we  have  seen  that  the  cortex  of  the  brain  forms  also  a 
common  centre  of  motor  connections,  a  motorium  commune,  and  that 
there  is  no  clear  dividing  line  between  the  common  sensory  and  common 
motor  centre ;  and  it  may,  therefore,  be  expected  that  the  disorders  of 
the  compound  feelings  will  not  be  separated  by  a  sharp  line  of  demar- 
cation from  the  disorders  of  the  compound  movements  of  the  body.  As 
a  matter  of  fact,  the  disorders  of  the  elementary  feelings,  of  the  com- 
pound feelings,  of  the  compound  movements,  and  of  the  elementary 
movements  merge  into  one  another  by  insensible  gradations,  and  it  is 
impossible  to  draw  anything  like  a  clear-cut  division  between  them. 
We  shall,  therefore,  describe  briefly  in  this  section  a  few  of  the  disorders 
of  the  compound  feelings  and  movements  under  the  name  of  psychical 
disorders,  and  without  attempting  to  differentiate  clearly  between  the 
two  sets  of  phenomena  : 

(1)  Pseudo-cesthesia  is  a  generic  name  given  to  sensations  and  per- 
ceptions experienced  in  the  absence  of  any  adequate  irritation  of  the 
peripheral  end-organs  or  of  the  conducting  paths,  the  condition  of  their 
production  being  a  molecular  discharge  from  the  common  sensory  centre. 
When  a  sensation  of  this  kind  is  experienced,  and  gives  rise  to  an 
erroneous  perception  of  external  objects  and  relations,  it  is  named  an 
illusion;  when  it  gives  rise  to  an  objective  sensation  in  the  entire 
absence  of  an  external  cause,  it  is  termed  a  hallucination ;  and  when 
the  patient  forms  such  a  distorted  conception  of  the  properties  and 
relations  of  things  actually  existing  that  he  is  led  to  a  false  conclusion 
with  regard  to  them,  the  condition  is  called  a  delusion. 

(2)  Unconsciousness.  —  The  molecular  activity  .of  the  sensorium 
commune  is  intermittent,  and  under  normal  conditions  it  is  suspended 
for  several  hours  every  night,  and  during  this  time  consciousness  is 
abolished.  This  constitutes  sleep.  If  the  subject  cannot  be  aroused 
to  consciousness  by  the  application  of  ordinary  stimuli,  the  condition  is 
called  somnolence  or  stupor ;  and  if  the  unconsciousness  become  so 
profound  that  the  subject  cannot  be  aroused  by  the  strongest  external 
stimuli,  the  condition  is  called  coma. 


136  GENEKAL    SYMPTOMATOLOGY. 

(8)  Subconscious  and  Semiconscious  Psychical  Actions. — Between 
the  active  consciousness  of  a  healthy  person  after  being  restored  l.y 
sleep  and  complete  insensibility  there  are  all  degrees  of  diminution  of 
sensibility.  It  is  well  known  that  a  person  whose  attention  is  strongly 
directed  to  a  particular  subject  is  insensible  to  ordinary  stimuli.  A 
more  advanced  degree  of  diminution  of  the  activity  of  consciousness  is 
manifested  by  persons  suffering  from  great  fatigue  and  loss  of  sleep. 
Under  such  circumstances  a  person  may  walk  about  in  a  half-conscious 
state,  and  a  similar  dazed  condition  is  frecjuently  observed  after  epileptic 
seizures.  The  patient  may  perform  complicated  motor  actions  Avhile  in 
a  totally  unconscious  condition,  as  is  seen  in  somnambulism,  the  mes- 
meric state,  or  the  narcosis  caused  by  chloroform  and  similar  agents. 

Unconscious  conditions  are,  indeed,  frequently  associated  with  motor 
disturbances.  When  the  inliil)itory  action  of  the  highest  coordinating 
centre  is  removed,  the  functional  activity  of  tlie  lower  centres  may  be 
increased.  Many  atrocious  murders  are  committed  during  the  period 
of  semiconsciousness  which  sometimes  follows  an  epileptic  seizure,  and  it 
is  well  kuoAvn  how  fierce  and  brutal  many  men  ))ecome  during  the  semi- 
conscious condition  induced  by  alcoholic  excess.  In  delirium^  again, 
the  highest  form  of  consciousness  is  in  abeyance,  while  the  lower,  earlier 
organized  forms  are  abnormally  active.  The  patient,  for  instance,  is 
unable  to  sleep,  and  yet  he  is  only  partialh^  conscious  of  surrounding 
objects  and  events ;  he  is  subject  to  illusions,  hallucinations,  and  delu- 
sions, and  motor  disturbances  are  manifested  bv  great  restlessness  and 
incoherent  speech.  It  is  probal)le  that  in  delirium  the  stock  of  irritable 
matter  in  the  gray  substance  of  the  cortex  is  much  exhausted,  and  that 
what  remains  manifests  an  undue  degree  of  irritability,  so  that  the 
protoplasm  gives  out  energy  either  spontaneously  or  on  the  application 
of  slight  stimuli,  while  functionally  there  is  a  dissolution  from  the  later 
to  the  earlier  acquired  feelings  and  experiences. 

But  although  the  patient  is  only  semiconscious  in  delirium,  yet  his 
mental  experiences  during  that  time  may  be  subsequently  remembered 
with  painful  intensity.  This  also  occurs  in  dreams.  The  patient  is 
wholly  unconscious  of  external  impressions  at  the  time,  but  he  is  par- 
tially conscious  of  a  succession  of  feelings  and  images,  cither  of  a 
joyful  or  a  painful  kind,  which  may  be  subsequently  revived  in  memory 
with  greater  vividness  than  almost  any  of  his  mental  experiences  during 
waking  hours.  Dreams  are  frequently  accompanied  by  motor  disturb- 
ances, such  as  vocalization  and  articulate  sounds.  The  most  prominent 
feature  of  the  night-terrors  of  children  is  the  outward  expression  of 
extreme  terror  by  which  the  attack  is  manifested.  The  partial  uncon- 
sciousness which  precedes  or  follows  an  epileptic  seizure  is  often  asso- 


SECONDARY    OK    COMPOUXD    .ESTH  ESIONEUROSES .      137 

ciated  with  the  (nitward  manifestations  of  one  of  the  emotions,  and 
sometimes  by  a  corresponding  inward  feeling.  The  aura  of  an  epileptic 
attack  may  be  a  guilty  expression,  and  the  patient  may  subsequently 
be  able  to  remember  that  innnediately  before  the  attack  he  experienced 
a  feeling  as  if  he  had  been  guilty  of  an  infamous  action.  What  appears 
to  be  an  increase  of  consciousness  often  results  from  a  diminished  activity 
of  the  higher  sentient  centres.  Increase  of  the  normal  desires  and 
appetites  sometimes  results  from  a  ])eripheral  irritation,  but  a  person  is 
liable  to  an  illegitimate  indulgence  of  the  passions  when  the  moral 
feelings  are  weakened,  and  tem])tation  is  apt  to  be  strongest  during 
states  of  mental  enfeel)lement  from  cerebral  exhaustion.  It  is  then 
also  that  remorse  for  previous  indulgence  is  liable  to  become  (|uite  dis- 
proportionate in  its  intensity  to  the  degree  of  guilt,  and  may  be  experi- 
enced in  the  absence  of  any  guilt  to  atone  for.  The  depressing  emotions, 
such  as  fear  and  anger,  are  also  liable  to  become  excessive  during  states 
of  nervous  exhaustion,  and  it  is  a  nuxtter  of  common  ol)servation  that  a 
person  who  is  in  feeble  healtli  is  often  very  irascible,  while  others  are 
easily  excited  to  laughter  or  tears.  Experiments  on  animals  have  show  n 
that  a  nerve  whose  nutrition  is  lowered  discharges  its  energy  more 
readily  than  one  whose  nutrition  is  perfect,  and  similarly  when  the 
nutrition  of  the  sensorium  commune  is  defective  it  responds  to  stimuli 
of  less  intensity  than  Avhen  its  nutrition  is  normal. 

(4)  Double  Consciousness!  ;  Periodic  Amnesia. — Closely  allied  to 
somnambulism  and  the  mesmeric  sleep  is  the  curious  condition  which 
has  been  called  double  consciousness,  or  periodic  amnesia.  In  this  con- 
dition the  subject  is  liable  to  periodic  seizures,  which  may  last  from 
some  hours  to  as  many  days,  and  during  which  there  is  complete  for- 
getfulness  of  the  feelings  and  events  of  ordinary  existence,  although 
rational  thou<>;lit  and  action  still  remain. 

(5)  Abnormal  States  of  Conscious7iess. — There  are  some  abnormal 
elementary  feelings  which  must  be  regarded  as  qualitative  rather  than 
quantitative  alterations  of  consciousness.  As  examples  of  these,  may 
be  mentioned  ('/)  headaclie,  (b)  vertigo,  and  (c)  fainting.  To  the  con- 
sideration of  these  nuiy  be  added  a  few  remarks  on  {d)  abnormal  appe- 
tites and  emotions. 

(a)  Headarhe. — Although  headache  is  an  excess  of  painful  feeling, 
yet  it  cannot  as  a  rule  be  regarded  as  an  excess  of  any  normal  feeling, 
or  of  any  feeling  which  can  be  excited  by  the  application  of  external 
stimuli.  From  this  statement  neuralgic,  rheumatic,  and  pro])a))ly 
some  other  forms  of  headache  must  be  excepted,  but  what  is  generally 
known  as  a  nervous  headache  is  a  truly  abnormal  feeling,  and  must  be 
experienced  by  a  person   before  he  can  form  an  adequate  idea  of  it. 


138  GENERAL    SYMPTOMATOLOGY. 

Such  headaches  are  caused  by  changes  of  circulation  in  the  brain,  the 
circulation  of  poisons  in  tlie  blood,  or  they  may  arise  spontaneously  at 
recurrino-  intervals.  It  is  probable  that  in  all  of  them  there  is  an 
alteration  of  tlie  irritability  of  the  cells  and  fibres  of  the  sensorium. 
Recurring  headaches  are  generally  associated  with  vaso-motor  phe- 
nomena in  the  regions  of  distribution  of  the  cervical  sympathetic 
nerves,  but  it  is  probable  that  these  are  the  results  and  not  the  cause 
of  the  sensorial  disturbance.  Such  headaches  are  regarded  by  Dr. 
Hughlings  Jackson  as  a  sensory  epilepsy  and  as  being  dependent  upon 
a  discharge  from  the  sensory  portion  of  the  cortex  of  the  brain. 

{!))  Vertigo  is  a  sensation  of  swimming  in  the  head,  during  which 
surrounding  objects  appear  to  oscillate  before  the  eyes,  or  rotate  in  a 
definite  direction,  and  which  is  also  accompanied  by  a  sense  of  stag- 
gering or  of  rotation  of  the  body.  A^ertigo  a})pears  to  be  the  subjec- 
tive correlation  of  want  of  coordination  between  the  various  muscular 
contractions  necessary  for  adjusting  the  body  to  the  different  objects 
which  surround  it  in  space.  It  is  a  prominent  symptom  of  those  dis- 
eases in  which  the  automatic  mechanism  for  maintaining  the  erect 
posture  is  deranged,  such  as  affections  of  the  cerebellum  and  Meniere's 
disease.  The  position  of  the  body  in  space  is  largely  determined  by 
the  association  of  objects  seen  with  the  appreciation  of  the  position  of 
the  eyes  and  head.  Displacement  of  the  positi(m  of  the  eyes,  such  as 
occurs  in  paralysis  of  one  or  more  of  the  recti  muscles,  or  of  the  posi- 
tion of  the  head,  such  as  occurs  in  rotation  of  the  head  with  conjugate 
deviation  of  the  eyes,  and  in  the  compulsory  movements  to  be  subse- 
quently described,  is  also  accompanied  by  severe  vertigo.  This  symp- 
tom frequently  attends  visceral  disease,  as  dyspepsia,  and  it  is  then 
probably  caused  by  vaso-motor  changes  influencing  the  cerebral  circula- 
tion. This  opinion  is  rendered  all  the  more  probable  from  the  fiict 
that  vertigo  is  a  troublesome  symptom  both  of  ansemia  and  congestion 
of  the  brain.  Vertigo  is  usually  accompanied  by  a  motor  phenomena 
in  the  region  of  distribution  of  the  pneumogastric,  such  as  feeble  and 
irregular  pulse,  irregular  respiration,  and  vomiting. 

(f)  Fainting  is  a  deadly  feeling  caused  by  sudden  anaemia  of  the 
brain  occasioned  by  severe  loss  of  blood  or  cardiac  failure.  It  also 
is  attended  by  gasping  respiration,  and  frequently  accompanied  by 
vomitino;. 

{d)  Ab>ior)nal  Appetites,  Amotions,  and  Impulses. — Drunkenness 
may  be  regarded  as  an  abnormal  appetite,  especially  when  it  assumes 
the  aggravated  form  of  dipsomania  ;  but  the  most  remarkable  example 
of  an  abnormal  appetite  is  afforded  by  the  condition  described  by 
Westphal  and  others  as  perverted  sexual  instinct  (contrare  sexualemp- 


SECONDAET    OR    COMPOUND    .ESTHESIONEUROSES .      139 

fimlung).  This  condition  is  defined  by  Westphal  as  "a  congenital 
perversion  of  the  sexual  instinct  with  retained  consciousness  of  the 
morbid  nature  of  the  condition,"  and  the  recorded  cases  show  that 
some  pei'sons  are  attracted  in  their  sexual  desires  exclusively  by  indi- 
viduals of  their  own  sex.  The  most  remarkable  of  the  abnormal 
emotions  consist  of  a  morbid  dread  experienced  in  the  absence  of  any 
circumstance  or  event  which  could  l)e  thought  in  the  remotest  deoree 
capable  of  inducing  such  a  feeling.  Some  persons  experience  an  un- 
conijuerable  feeling  of  dread  when  they  are  alone  in  an  open  space 
[am/oraphohia) ;  others  have  the  same  feeling  when  in  a  narrow  lane 
between  two  Avails  {claustrophobia).  Some  people  have  a  morbid  dread 
of  society  (anthrophohia),  while  there  are  some  men  who  only  experi- 
ence an  aversion  to  the  society  of  women  {(lynephohia).  Some  persons 
are  totally  unable  to  sign  their  names  in  the  presence  of  a  witness.  A 
gentleman  in  business  once  told  me  that  while  able  to  keep  accounts 
and  attend  to  his  business  as  well  as  ever,  he  found  himself  totally 
unal)le  to  sign  a  check  if  his  clerk  made  a  sudden  demand  for  one. 
Suicidal,  homicidal,  and  other  morbid  impulses  are  liable  to  become 
uncontrollable  during  periods  of  great  nervous  exhaustion,  and  when 
the  highest  manifestations  of  consciousness  are  in  abeyance.  Atrocious 
crimes  are  usually  committed  by  persons  during  the  period  of  depres- 
sion which  follows  a  prolonged  carouse,  or  when  the  individual. is  in 
a  state  of  semi-stupefaction,  either  from  alcohol  or  as  a  sequel  to  an 
epileptic  seizure. 


CHAPTER    Y. 

GENERAL  SYMPTOMATOLOGY  {continued). 
B.  TKOPHONEUROSES. 

The  degenerations  of  the  nervous  system  having  ah-eady  been  con- 
sidered, we  shall  now  proceed  to  describe  the  degeneration  of  muscles 
which  result  from  nervous  disease. 


I.  Neueotic  Atrophy  of  Muscle. 

Neurotic  atrophy  of  muscle  may  be  divided  into  three  stages, 
namely:  1,  Simple  atrophy;  1,  Atrophy  with  nuclear  proliferation; 
3,  Cirrhosis  of  muscle. 

1.  Simple  Atrophy. 

In  simple  atrophy  and  the  early  stage  of  the  severer  forms  of 
atrophy,   the  muscular   fibres   undergo   a  simple    diminution   in   size, 


t         ■     c 

Atrophv  of  Muscular  Fibres  from  a  Case  of  Infantile  Paralysis.     (After  Havem.) 
«,  Fibres  of  normal  size,  showing  multiplication  of  nuclei ;  6,  simple  atrophy,  with  granular  degenera- 
tion ;  c,  advanced  granular  degeneration,  with  atrophy. 

without  presenting  any  degenerative  changes.     The  longitudinal  and 
transverse  striations  are  at  times  as  well  preserved  as  in  health  (Fig. 


NEUROTIC    ATROPHY    OF    MUSCLE.  141 

G4,  a),  and  not  a  trace  of  fatty  degeneration  can  be  discovered.  It 
would  appear  that  the  fibrilhe  of  which  the  fibre  consists  are  diminished 
in  number,  but  those  which  remain  do  not  seem  to  be  sensibly  dimin- 
ished in  size.  At  other  times  the  striation  becomes  less  marked  and 
more  delicate  than  in  health,  probably  owing  to  a  diminution  in  the 
length  of  the  sarcous  elements  of  the  contractile  disks  (Fig.  G-t,  h). 
The  substance  of  the  contractile^  disks  may  also  present  a  finely  granu- 
lar aspect,  which  appears  to  be  the  first  indication  of  the  profound 
chemical  change  which  this  substance  subsequently  undergoes. 

2.  Atrophy  with  Xud'ar  Proliferation. 

When  the  muscle  is  examined  from  three  to  five  weeks  after  the 
injury  the  contents  of  the  fibre  are  now  seen  to  have  undergone  a  finelv 
granular  degeneration  (Fig.  64,  c).  The  granules  at  first  consist  of 
altered  protein,  but  they  soon  become  distinctly  fatty.  The  primitive 
fibrils  now  disappear,  and  only  small  fragments  of  the  fibre  present, 
here  and  there,  either  transverse  or  longitudinal  striation.  In  addition 
to  these  changes  the  nuclei  or  muscle  corpuscles  are  multiphetl.  and  in 
the  later  stages  of  atrophy  the  sarcolemma  may  become  almost  filled 
Avitli  masses  of  nuclei  Avhich  are  surrounded  by  granular  and  fatty 
detritus,  while  the  contents  of  the  fibres  are  completely  disintegrated 
(Fig.  65,  h  h).  The  nuclei  of  the  endomysium  also  seem  to  be  more 
numerous  than  in  health. 

3.    Cirrhosis  of  Muscle. 

The  nuclei  of  the  endomysium,  now  greatly  increased  in  number, 
elongate  into  fibres  which  form  narrow  bands  of  fibrous  tissue  running 
parallel  to  the  direction  of  the  muscular  fibres,  and  cicatricial  contrac- 
tion of  this  tissue  completely  destroys  the  remnants  of  muscular  fibre 
and  gives  rise  to  organic  shortening  of  the  l)and  of  fibrous  tissue  which 
now  represents  the  muscle.  These  bands  of  filirous  tissue  contain 
many  oat-shaped  nuclei  and  connective-tissue  cells  (Fig.  65,  a  a)  which 
may  become  distended  with  flit,  and  these  fat  cells  may  become  so 
abundant  that  the  original  volume  of  the  muscle  may  be  maintained  or 
even  exceeded. 

It  is  now  fully  ascertained  that  active  neurotic  atrophy  of  muscle 
never  occurs  except  when  the  spino-neural  mechanism  is  injured,  either 
by  disease  of  the  ganglion  cells  of  the  anterior  horns  of  the  cord  and 
the  corresponding  cells  in  the  medulla  oblongata  and  pons,  or  of  the 
efferent  fibres  which   connect   these   with   the  muscles.     A   moderate 


142 


GENERAL    SYMPTOMATOLOGY, 


decrree  of  muscular  atrophy  may  also  be  caused  by  irntation  of  the 
afferent  fibre  of  the  reflex  arc.  Whether  the  same  cell  exercises  both 
trophic  and  motor  functions,  or  there  exist  separate  cells  for  each  func- 
tion is  as  yet  undetermined.  It  would  appear  that  a  destructive  lesion 
of  the  cranglion  cells,  or  of  the  efferent  fibres  which  connect  these  with 
the  muscle,  causes  both  motor  paralysis  and  active   atrophy,  while  in 

Fig.  65. 


Infantile  Paralysis.     (After  Havem.) 

a  a,  Excess  of  connective  tissue,  containing  a  large  number  of  conuective-tisBue  and  fat  cells  ;  6  b,  atro- 

pliied  muscular  fibres,  containing  a  large  number  of  nucli^i  ;  c,  simple  atrophj-  of  muscular  filjre 


severe  cases  there  is  also  rapid  loss  of  the  faradic  contractility.  A. 
certain  degree  of  wasting  may  occur  in  paralyzed  muscles  Avhen  the 
lesion  is  restricted  to  the  cerebral  mechanism,  but  this  form  of  atrophy 
arises  simply  from  disease  of  the  muscle,  and  differs  entirely  from  the 
active  atrophy  which  has  just  been  described. 


CUTANEOUS    TROPHIC     AFFECTIONS.  143 

II.  Cutaneous  Trophic  Affections. 

1.   Ciititneous  Eruptions  in  Lesions  of  Peripheral  Nerves. 

Erythematous  patches  are  often  observed  on  the  extremities  after 
traumatic  lesions  of  the  peripheral  nerves,  on  the  root  of  the  nose  and 
forehead  in  trigeminal  neuralgia,  and  on  the  hand  in  cases  of  brachial 
neuralgia.  Erythema  often  arises  in  the  course  of  digestive  disorders, 
and  it  is  then  most  probably  of  reflex  origin.  The  urticaria  which  is 
caused  by  the  stings  of  insects  and  nettles,  and  that  which  arises  in  the 
neighborhood  of  the  puncture  in  subcutaneous  injections,  seems  to 
indicate  that  this  eruption  is  often,  if  not  always,  of  nervous  origin. 
Vesicular  eruptions  are  often  observed  after  injury  to  nerves.  Ecze- 
matous  eruptions  are  often  associated  with  neuralgic  pains  in  the  area 
of  distribution  of  an  injured  nerve,  and  eczema  of  the  whole  side  of 
the  face  has  been  observed  to  accompany  a  severe  attack  of  trigeminal 
neuralgin.  Herpes  zoster  often  accompanies  a  severe  attack  of  neuralgia. 
Its  favorite  seat  is  the  skin  covering  one  or  more  of  the  intercostal 
spaces,  and  the  neuralgia  which  accompanies  it  generally  begins  and 
terminates  with  the  eruption  ;  but,  in  aged  people,  the  pain,  which  is 
very  intractable,  continues  long  after  the  eruption  has  disappeared. 
Herpes  zoster  of  the  face  occurs  in  trigeminal  neuralgia.  It  may 
appear  on  any  part  of  the  face,  but  is  most  frequent  on  the  forehead. 
When  the  palpebral  nerves  are  affected  the  eruption  spreads  over  the 
upper  eyelid,  and  the  conjunctiva  is  inflamed  ;  and  when  the  frontal  and 
its  nasal  branches  are  likewise  involved,  the  iris  and  other  structures 
within  the  eyeball  are  inflamed,  and  the  disease  may  then  cause  serious 
damage  to  the  eye.  Herpes  zoster  has  also  been  observed  in  the  area  of 
distribution  of  various  spinal  sensory  nerves  when  the  nerve  is  com- 
pressed by  aneurism,  cancer  of  the  vertebra,  or  other  tumors.  Evidences 
of  neuritis  of  the  aifected  intercostal  nerves  have  been  found  in  cases  that 
died  whilst  the  patients  were  suffering  from  intercostal  herpes  zoster. 
Pemphigus  bulh^  sometimes  develop  with  great  rapidity  over  various 
parts  of  the  surface  supplied  by  the  cutaneous  branches  of  an  injured 
nerve.  After  section  or  injury  of  nerves,  the  skin  frequently  becomes 
dry,  harsh,  and  scaly  ;  and  a  case  is  reported  by  Eulenburg  in  which 
several  branches  of  the  brachial  plexus  were  injured  and  compressed  in 
consequence  of  a  dislocation  of  the  humerus,  and  in  which  ichthyosis 
of  the  skin  of  the  affected  extremity  had  supervened. 

After  traumatic  injuries  of  nerve-trunks  the  skin  often  undergoes 
atrophy,  loses  its  Avrinkles,  and  becomes  smooth  and  glossy,  and  conse- 


144  GENEKAL    SYMPTOMATOLOGY. 

quently  this  condition  has  been  named  "  glossy  skin  "  by  Paget.  "  In 
well-marked  cases,"  this  author  says,  ''  the  fingers  Avhich  are  affected 
(for  this  appearance  may  be  confined  to  one  or  two  of  them)  are  usually 
tapering,  smooth,  hairless,  almost  void  of  wrinkles,  glossy,  pink  or 
ruddy,  or  blotched  as  with  permanent  chilblains.  They  are  commonly 
also  very  painful,  especially  on  motion,  and  pain  often  extends  from 
them  up  tlie  arm."  Glossy  skin  is  often  met  with  in  injuries  of  the 
ulnar  nerve  of  the  brachial  plexus  and  in  the  upper  extremity  ;  the 
palm  of  the  hand  is  the  part  which  usually  suffers,  while  in  injuries  of 
the  nerves  of  the  lower  extremity  the  dorsum  of  the  foot  appears  to  be 
the  part  most  liable  to  be  attacked.  Patches  of  leucoderma,  with 
aneesthesia  of  the  affected  skin,  have  been  observed  on  the  face  in 
trigeminal  neuralgia,  and  over  other  parts  of  the  body  after  injuries  to 
large  nerve  trunks.  Patches  of  highly  pigmented  skin,  with  anaesthesia, 
have  also  been  found  scattered  irregularly,  but  symmetrically,  all  over 
the  body  ;  these  also  being  doubtless  of  nervous  origin. 

The  early  occurrence  and  the  severe  degree  of  anaesthesia  in  the 
tubercular  variety  of  leprosy,  as  well  as  the  manner  in  which  it  pro- 
gresses from  the  periphery  towards  the  central  parts  of  the  affected 
limbs,  Avould  alone  indicate  that  disease  of  some  part  of  the  nervous 
system  is  a  prominent  part  of  the  affection,  and  characteristic  anatomical 
changes  have  been  found  in  the  nerve-trunks.  Morbid  changes  have 
also  been  discovered  in  the  spinal  cord  and  brain,  but  it  is  probable 
that  disease  of  the  nerve-trunks  takes  the  most  active  part  in  causing 
the  local  symptoms. 

2.   Cutaneous  Eruptions  in  Diseases  of  the  Spinal  Cord. 

Cutaneous  eruptions  of  various  kinds  occur  in  cases  of  chronic  mye- 
litis, but  they  are  most  frequently  met  with  during  attacks  of  lightning 
pains  in  tabes  dorsalis.  These  eruptions  consist  of  patches  of  urticaria, 
vesicular  eruptions  of  which  herpes  is  the  most  common,  and  papular 
eruptions  like  lichen  planus,  and  they  ai-e  always  limited  to  nerve  terri- 
tories affected  with  neuralgic  and  lightning  pains.  Several  cases  of  pem- 
phigus in  connection  with  spinal  disease  have  been  recorded  by  Chovstek 
and  olhers.  A  case  is  recorded  l)y  Balmer  in  which  an  attack  of  pem- 
phigus occurred  in  the  course  of  progressive  muscular  atrophy. 

3.  Cutaneous  Eruptions  in  Diseases  of  the  Brain. 

Herpes  is  not  infrequently  associated  with  hemiplegia,  but  it  is 
doubtful  whether  there  is  anything  more  than  an  accidental  connection 
between  them.     Two  cases  are  reported  bv  Dr.  Duncan,  in  each  of 


TROPHIC    DISORDERS    OF     THE    XAILS    AXD    HAIR.       l-i.") 

Avliich  an  eruption  of  herpes  appeared  on  the  affected  side  simulta- 
neously with  the  motor  paralysis.  Several  cases  are  reported  in  which 
a  pemphigus  eruption  appeared  on  one  of  the  paralyzed  extremities  in 
hemiplegia  of  central  origin. 

III.  Trophic  Disorders  of  the  Nails  and  Hair. 

1.  Trophic  Disorders  of  the  Nails  and  Hair  in  Lesions  of  the 

Nerve-trunks. 

Traumatic  lesions  of  nerve-trunks  in  which  the  nerve  is  not  com- 
pletely divided,  are  followed  by  various  deformities  of  the  nerves.  The 
nails  become  greatly  curved — both  laterally  and  longitudinally — fur- 
rowed, dry,  and  cracked  at  their  extremities,  and  of  a  yellowish-brown 
color.  These  deformities  may  also  occur  in  connection  with  neuralgia 
and  idiopathic  neuritis  of  sensory  nerve-trunks.  Local  affections  of 
the  hair  often  occur  in  man  after  traumatic  lesion  of  nerve-trunks,  or 
in  connection  with  idiopathic  neuritis  and  neuralgia.  The  hairs  over 
the  region  of  distribution  of  a  nerve  affected  with  neuralgia  have  some- 
times been  observed  to  be  hypertrophied  and  even  increased  in  number  ; 
but,  as  a  rule,  the  effect  of  neuralgia  upon  the  hair  is  to  make  it  brittle, 
and  to  cause  it  to  fall  out  in  considerable  quantities.  Localized  gray- 
ness  of  the  hair  is  often  associated  with  ophthalmic  neuralgia,  and  it 
may  also  involve  the  eyebrow  of  the  affected  side.  This  grayness 
sometimes  assumes  an  intermittent  character,  increasing  during  and 
sometimes  after  an  acute  attack  of  pain,  the  color  becoming  partially 
restored  in  the  interval  between  the  paroxysms.  In  glossy  skin  the 
surface  becomes  hairless. 

2.  Trophic  Disorders  of  the  Nails  and  Hair  in  Spinal  Disease. 

The  nails  may  become  deformed  in  cases  of  acute  and  chronic 
myelitis,  but  the  most  remarkable  change  to  which  they  are  liable  in 
spinal  diseases  occurs  in  locomotor  ataxia.  In  the  course  of  this  disease 
the  nails  of  the  great  toes  sometimes  fall  oft"  spontaneously,  and  are  then 
rapidly  replaced  by  a  new  and  perfectly  normal  nail,  which  may  In  its 
turn  ftill  off  a  few  months  later,  and  this  process  may  occur  in  the 
same  nail  several  times  in  succession.  The  falling  off  of  the  nail  may 
be  preceded  for  some  weeks  by  a  dull  pain,  or  by  a  feeling  of  uneasi- 
ness in  the  toe,  and  then  the  nail  falls  oft'  without  being  accompanied 
either  by  suppuration  or  by  apparent  ulceration  of  the  matrix.  In 
other  cases  the  patient  observes  that  the  nail  of  one  great  toe,  and  a 
few  days  later  that  of  the  other,  suddenly  become  of  a  dark  blue  color 

10 


146  GENERAL    SYMPTOMATOLOGY. 

from  subungual  effusion  of  blood,  and  a  few  days  afterwards  the  nail 
falls  off,  witliout  being  preceded  or  accompanied  by  pain  or  other  warn- 
ing. The  nails  have  also  been  known  to  fall  off  in  sclerosis  in  patches. 
An*  increased  growth  of  hair  has  occasionally  been  observed  in  cases  of 
chronic  myelitis. 

3.   Trophic  Disorders  of  tJie  Nails  and  Hair  in  Cerebral  Diseases. 
In  cases  of  hemiplegia  the  nails  become  curved  and  cracked,  but  the 
trophic  disorders  to  which  they  and  the  hair  are  liable  in  cerebral  dis- 
ease are  by  no  means  so  well  marked  as  in  spinal  affections  and  lesions 
of  nerve-trunks. 

IV.  Bej)Sores  and  other  Destructive  Processes. 

1,  Decubitus  Aeutus. — Some  days  or  even  hours  after  the  occurrence 
of  a  severe  spinal  or  cerebral  lesion,  or  aftei-  a  sudden  exacerbation  of 
these  affections,  one  or  several  erythematous  patches  appear  over  the 
sacrum  and  gluteal  regions,  the  trochanters  of  the  femur,  ankles,  or 
other  parts  subjected  to  pressure.  In  -these  patches,  which  are  of 
variable  extent  and  irregular  form,  the  skin  assumes  a  rosy  hue,  or 
becomes  dark  red  or  violet,  but  the  color  disappears  momentarily  on 
pressure  with  the  finger.  After  a  period  which  varies  from  twenty- 
four  to  forty-eight  hours,  the  central  part  of  the  erythematous  patch  is 
covered  with  vesicles  or  bullae,  the  contents  of  which,  at  first  colorless 
and  transparent,  become  more  or  less  opaque,  reddish,  or  brown  colored. 
Under  favorable  circumstances  the  vesicle  may  wither,  dry  u]),  and  dis- 
appear, and  the  part  recover  without  further  change;  but  in  most  cases 
the  vesicles  burst,  and  leave  ill-looking  ulcers,  the  bases  of  which  are 
composed  of  the  true  skin  in  a  state  of  ])hlegmonous  inflammation,  and 
infiltrated  with  blood.  The  base  of  the  ulcer  soon  perishes  by  gan- 
grene, the  neighboring  skin  becomes  inflamed  to  a  greater  and  greater 
extent,  and  the  gangrenous  destruction  extends  deeper  and  deeper, 
laying  bare  and  including  in  its  destructive  operation  muscles,  tendons, 
fiiscise,  hgaments,  and  even  the  subjacent  bones.  One  of  the  most  re- 
markable characteristics  of  the  affection  is  the  extreme  rapidity  of  its 
development,  the  entire  cycle  of  changes  being  completed  in  a  few  days. 
Cystitis  and  hsematuria  are  not  infrequent  complications  of  this  condi- 
tion, and  the  muscles  of  the  lower  extremities  become  the  subjects  of 
rapid  atrophy.  Metastatic  abscesses  now  occur  in  the  kidney,  lungs, 
and  other  viscera,  the  accompanying  fever  assumes  a  remittent  type, 
and  the  patient  dies  of  septic  fever.  In  some  cases  the  gangrenous 
process  extends  to  the  sacral  bones,  and  with  the  destruction  of  the 


BEPSdRES    AND    OTHER    DESTRUCTIVE    PROCESSES.      147 

sacro-coccygeal  ligament  the  vertebral  canal  is  opened,  and  thus  the 
ichorous  discharges  find  access  to  the  fatty  cellular  tissue  which  sur- 
rounds the  dura  mater,  and  by  penetrating  this  membrane  they  may 
even  make  their  Avay  to  the  arachnoid  cavity.  This  grave  accident  is 
followed  by  a  simple  purulent  or  an  ichorous  ascending  meningitis, 
which  rapidly  reaches  the  base  of  the  brain,  and  is  soon  fatal. 

2.  Chronic  Decubitus. — In  chronic  diseases  of  the  spinal  cord  the 
portions  of  skin  subjected  to  pressure  in  the  recumbent  posture  assume 
a  dark  red  color,  and  at  times  become  covered  with  superficial  ulcera- 
tions. After  a  time  a  black  spot  appears  on  the  reddened  portion  of 
skin,  and,  if  i)re8sure  is  contiimed,  it  enlarges  rapidly,  and  the  afiected 
skin  dries  up  into  a  hard  leathery  mass.  In  a  short  time  a  boundary 
line  of  inflamniation  forms  around  the  gangrenous  portion  of  skin,  and 
the  latter  may,  under  proper  treatment,  be  thrown  oif,  leaving  a  more 
or  less  healthy  granulating  surface,  which  may  sometimes  cicatrize. 
But  if  the  pressure  be  continued,  or  if  the  primary  disease  of  the  ner- 
vous system  undergo  a  fresh  exacerbation,  the  ulcerated  surface  assumes 
a  dark  violet  color,  the  gangrene  spreads  rapidly,  and  all  the  destructive 
changes  characteristic  of  acute  bedsore  make  their  appearance  and  soon 
lead  to  a  fatal  result. 

3.  SyrtDiietrical  Gangrene  and  Local  Asphyxia. — This  disease, 
which  was  first  described  by  Raynaud,  generally  involves  the  fingers, 
and  less  frequently  the  toes,  tips  of  the  nose,  and  external  ear.  The 
affected  parts  become  suddenly  white,  cold,  bloodless,  and  insensible, 
and  motor  power  is  diminished.  The  skin  is  wrinkled  and  shrunken, 
the  ends  of  the  fingers  appear  thin  and  conical,  and,  when  the  whole 
exti-emity  is  affected,  the  pulse  is  feeble  or  imperceptible.  After  some 
months  reaction  sets  in :  the  parts  then  become  congested,  of  a  violet 
or  livid  color,  intensely  painful,  and  the  seat  of  troublesome  itching, 
while  vesicles  form  which  are  filled  with  a  sero-purulent  fluid,  and,  on 
bursting,  leave  the  cutis  excoriated.  Even  at  this  stage  recovery 
may  take  place,  but  the  attack  usually  recurs,  and  ultimately  the  parts 
undergo  a  true  nmmmification  and  the  last  phalanges  of  the  fingers  drop 
off".  The  disease  occurs  usually  in  chlorotic  and  nervous  persons,  and 
is  seldom  met  with  in  children  and  old  people.  It  appears  to  be  caused 
by  a  spastic  ischtemia  of  the  arterioles. 

4.  Perforathig  Ulcer  of  the  Foot. — This  aff"ection,  as  seen  in  the 
foot,  is  less  like  an  ulcer  than  a  sinus.  It  usually  presents  itself  as  a 
small  aperture,  which  leads  directly  by  a  narrow  channel  to  exposed 
and  diseased  bone.  From  this  opening  there  is  little  or  no  discharge  ; 
the  skin  surrounding  the  orifice  is  greatly  thickened  by  superimposed 
layers  of  epidermis,  and,  indeed,  the  formation  of  a  large  corn  appears 


148  GENERAL    SYMPTOMATOLOGY. 

always  to  precede  the  destructive  process.  The  ulcer  is,  as  a  rule, 
insensible  to  ordinary  stimuli,  and  there  is  no  pain  when  the  patient  is 
at  rest ;  but  considerable  pain  may  be  caused  by  pressure  on  the  sole 
during  locomotion,  and  the  patient  often  suffers  from  severe  lightning 
painsln  the  lower  extremities.  Not  only  are  the  tissues  surrounding 
the  wound  insensible,  but  there  is  also,  as  a  rule,  more  or  less  complete 
cutaneous  anaesthesia  and  analgesia  of  the  whole  of  the  sole  of  the  foot, 
and  sensation  may  be  diminished  in  the  region  of  distribution  of  one 
or  more  of  the  cutaneous  nerves  as  far  up  as  the  calf  or  knee.  The 
surfiice  is  usually  cold  in  the  anaesthetic  area,  and  the  extremity  is 
likewise  apt  to  become  livid  on  slight  exposure,  Avhile  it  is  prone  to 
attacks  of  inflammation  or  of  eczema.  These  inflammatory  attacks 
sometimes  implicate  the  subcutaneous  tissues ;  the  limb  then  becomes 
greatly  swollen  and  oedematous,  and  the  attack  occasionally  termin- 
ates in  suppuration.  Lesions  of  the  articulations  of  the  foot  fre- 
quently accompany  this  affection,  and  not  only  is  the  joint  in  direct 
relation  with  the  wound  diseased,  but  it  is  also  not  uncommon  to  meet 
with  more  or  less  complete  ankylosis  of  all  tlie  phalangeal,  metatarso- 
phalangeal, and  tarso-metatarsal  articulations,  while  sul)luxations  of  these 
joints  may  take  place  in  other  cases.  It  is,  however,  pr()l)ab]e  that 
extensive  disease  of  the  bones  and  joints  of  the  foot  o»ily  occurs  when 
perforating  ulcer  is  a  symptom  of  locomotor  ataxia.  The  nails  assume 
a  brownish  color ;  they  become  greatly  thickened,  curved  longitudinally 
and  laterally,  furrowed,  dry,  and  cracked.  The  skin  of  the  leg  be- 
comes at  times  pigmented,  and  there  is  an  increase  in  the  growth  of 
the  hair,  while  the  foot  is  bathed  in  sweat  which  has  a  permanently 
fetid  odor.  The  ulcer  is  generally  situated  over  the  metatarso-phalan- 
geal  articulations,  most  frequently  over  those  of  the  big  and  little  toes. 
There  may  be  as  many  as  three  ulcers  on  one  foot,  and  when  both  feet 
are  affected  the  disease  is  generally  symmetrical.  Perforating  ulcer 
has  on  rare  occasions  been  met  with  in  the  hands.  The  disease  is 
essentially  chronic;  the  ulcers  may,  under  favorable  circumstances, 
remain  stationary  for  a  long  time,  and  may  even  heal  under  prolonged 
rest,  but  a  relapse  readily  occurs  Avhen  the  patient  begins  to  walk. 

The  most  recent  observations  on  perforating  ulcer  of  the  foot  show 
that  it  is  very  frequently,  if  not  always,  associated  with  other  symptoms 
of  locomotor  ataxia.  It  was  known  a  long  time  ago  that  this  form  of 
ulcer  was  often  accompanied  by  shooting  pains  and  anaesthesia  in  the 
lower  extremities,  while  strabismus  and  other  ocular  troubles  Avere  also 
mentioned  as  being  present  in  such  cases.  It  is  now  found  that  patients 
with  perforating  ulcer  also  suffer  from  gastric  crises,  arthropathies, 
swaying  movements  on  closing  the  eyes,  tottering  or  unsteady  gait,  and 


BEDSORES    AND    OTHER    DESTRUCTIVE    PROCESSES.       149 

absence  of  the  patellar-tendon  reactions.  Perforating  ulcer  is  associated 
with  the  neuralgic  form  of  locomotor  ataxia,  and  motor  disorders  do 
not  form  prominent  features  of  such  cases.  It  may  be  one  of  the 
earliest  symptoms  of  the  disease,  and  may  even  precede  the  anesthesia 
of  the  loAver  extremities,  so  that  its  association  with  locomotor  ataxia 
is  not  always  readily  made  out.  In  a  case  wliich  was  under  the  care 
of  my  colleague,  Mr.  Hardie,  there  was  some  degree  of  anaesthesia  of 
the  lower  extremities,  but  the  patellar-tendon  reactions  were  exagger- 
ated, and  I  was  about  to  conclude  that  the  case  was  not  one  of  loco- 
motor ataxia,  A  closer  examination,  however,  showed  that  the  patient 
had  suffered  from  diplopia,  and  that  the  pupils  failed  to  react  to  light, 
but  reacted  to  accommodation.  The  presence  of  these  symptoms  ren- 
dered it  very  probable  that  the  patient  was  in  the  early  stage  of  loco- 
motor ataxia,  notwithstanding  the  patellar-tendon  reactions  were  ex- 
aggerated. Dengenerative  lesions  of  the  nerves  have  been  found,  on 
microscopical  examination,  in  several  cases  of  perforating  ulcer. 

5.  Unilateral  Profiremive  Atrophy  of  the  Face  {Heniiatrophia 
Facialis  Progressiva). — This  disease  has  been  observed  about  twice  as 
often  in  women  as  in  men,  and  it  generally  begins  between  10  and  15 
years  of  age,  although  it  has  occasionally  been  observed  as  early  as  2 
and  as  late  as  30  years  of  age.  The  characteristic  phenomena  of  this 
disease  may  be  preceded  for  some  time  by  such  symptoms  as  a  local 
herpetic  eruption,  toothache,  tearing  pains  in  the  head  and  superior 
maxillary  region,  ei)ileptiform  attacks  in  which  the  spasms  are  some- 
times more  or  less  limited  to  the  side  of  the  face,  an  attack  of  hemi- 
plegia, spasms  of  tlie  masticatory  muscles,  and  hypersesthesia  with 
parsesthesia  in  the  side  of  the  face,  which  is  afterwards  the  subject  of 
atrophy. 

The  first  definite  symptom  to  attract  notice  is  a  peculiar  discolora- 
tion of  circumscribed  areas  of  the  skin.  Small  spots  of  a  white  color 
and  slightly  depressed  appear  on  the  side  of  the  face,  and  these  gradu- 
ally spread  so  as  to  coalesce  into  a  patch  of  considerable  size.  The 
affected  area  may  now  assume  a  yellowish  or  brownish  tint  like  that 
often  observed  in  cicatrices  after  burns,  the  skin  over  them  becomes 
thin  and  emaciated,  the  subcutaneous  fat  disappears,  and  the  side  of 
the  face  becomes  deformed  by  pits  of  greater  or  less  size  and  depth. 
On  the  affected  side  the  eyeball  often  sinks  back  into  the  orbit  from 
disappearance  of  the  orbital  fit,  the  palpebral  fissure  is  narrowed,  tiie 
beard,  eyelashes,  and  hair  of  the  head  become  gray  and  undergo 
other  structural  changes,  and  the  secretions  of  the  sebaceous  follicles  is 
arrested,  but  the  functions  of  the  sweat  glands  appear  to  be  normally 


l^Q  GENEKAL    SYMPTOMATOLOGY. 

performed.  lu  advanced  cases  the  affected  skin  feels  irregular  and 
atrophied,  and  it  may  assume  the  form  of  a  cicatrix,  but  does  not 
become  adherent  to  the  underlying  structures.  Cutaneous  sensibility 
is  not,  as  a  rule,  much  affected,  hut  patients  sometimes  complain  of 
various  parfesthesise  in  the  atrophied  portions  of  skin,  and  others  have 
suffered  from  neuralgiform  attacks,  while  in  one  case  partial  ani^sthesia, 
and  in  a  few  others  hypertesthesia  was  present. 

The  muscles  are  not  usually  implicated  in  the  atrophy,  but  in  a  case 
observed  by  Eulenburg  and  Guttmann  the  masticatory  muscles  on  the 
affected  side  were  relatively  feeble  and  emaciated,  in  a  few  cases 
atrophy  of  one  half  of  the  orbicular  of  the  mouth  w^as  observed,  and 
in  other  cases  one  half  of  the  tongue,  the  veil  of  the  palate,  and  the 
uvular  were  found  atrophied,  but  the  muscles  always  gave  normal  elec- 
trical reactions.  Romberg  reports  a  case  occurring  in  an  unmarried 
woman,  aged  twenty-eight  years.  The  left  side  of  her  face  had  gradu- 
ally atrophied  as  the  result  of  extensive  suppuration  on  the  left  side  of 
the  neck,  which  had  burst  through  the  tonsil.  Every  feature,  including 
the  brow,  eye,  nostril,  lips,  cheek,  and  chin,  as  well  as  the  left  half  <»f 
the  tongue  and  left  arch  of  the  palate,  was  smaller  than  those  on  the 
opposite  side. 

The  large  arteries  of  the  face  are  generally  unaltered  in  size,  and 
the  tone  of  the  small  arteries  is  retained  or  increased.  The  atrophied 
parts  are  generally  capable  of  blushing,  and  also  redden  under  local 
electrical  excitation.     The  temperature  is  the  same  on  both  sides. 

The  bones  of  the  face  liave  been  found  decidedly  diminished  in 
volume.  The  upper  and  lower  maxillary  Ijones  and  the  cartilages  of 
the  nose  are  often  atrophied,  especially  Avhen  the  disease  begins  at  an 
early  age.  Romberg  was  the  first  to  give  an  accurate  description  of 
this  affection,  and  he  classified  it  amongst  the  trophoneuroses.  The 
trophic  fibres  are  not  likely  to  run  in  the  motor  branch  of  the  fifth 
nerve,  inasmuch  as  paralysis  and  atrophy  of  the  masticatory  muscles, 
although  occasionally  present,  are  never  prominent  symptoms.  Cases 
have  been  described  by  Seeligmiiller  and  Brunner,  in  which  the  symp- 
toms appeared  to  have  been  caused  by  disease  of  the  cervical  sympa- 
thetic, but  it  is  probable  that,  as  suggested  by  Miiller,  the  lesion  is 
situated  in  the  medulla  oblongata.  This  disease  is,  with  occasional 
long  pauses  and  recommencements,  a  progressive  one,  and  no  treatment 
has  hitherto  been  of  any  avail. 

6.  Neuroparalytic  Ojjhthahnia.—Tlm  affection  begins  with  conges- 
tion of  the  conjunctiva,  which  is  followed  by  profuse  secretion  of  mucus 
or  pus,  nisensibility  and  opacity  of  the  cornea,  and  a  pseudo-mem- 
branous exudation  of  the  iris.     In  a  few  days  ulceration  and  perfora- 


ARTICULAR    AXD    OSSEOUS    AFFECTIONS  151 

tion  of  the  cornea  may  oecuv,  -which  is  followed  by  escape  of  the 
humors  and  collapse  of  the  eye. 

Several  hypotheses  have  been  advanced  to  account  for  this  destruc- 
tive inflammation  of  the  eyeball,  but  the  most  probable  is  that  it  is 
due  to  irritation  of  the  trophic  fibres  which  descend  from  the  casserian 
tranulion  to  the  eyeball. 

7.  Simple  Glaueovia. — Experiments  on  animals  have  shown  that 
irritation  of  the  nucleus  of  the  trigeminus  in  the  medulla,  or  of  the 
nerve  itself,  is  foUow^ed  by  increase  of  the  intraocular  pressure,  caused 
by  augmented  secretion  of  the  aqueous  humor.  As  a  result  of  the 
high  tension  the  iris  and  lens  are  pushed  forwards,  and  the  internal 
membranes  are  stretched.  It  is  supposed  by  many  pathologists  that 
glaucoma  is  produced  by  a  similar  mechanism,  although  this  opinion  is 
not  accepted  by  all. 

V.  Nutritive  Affections  of  the  Joints,  Bones,  and  Teeth 
(Articular  and  Osseous  Trophoneuroses). 

1.  Affections  of  Peripheral  Oruiin. — Traumatic  injuries  of  nerves,  in 
which  the  nerves  are  not  completely  divided,  are  often  followed,  any 
time  after  the  first  few  days,  by  disease  of  the  joints,  which  consists  of 
a  painful  swelling  like  that  of  subacute  articular  rheumatism.  This 
swelling  may  attack  any  or  all  of  the  articulations  of  a  limb,  and  often 
begins  in  the  joints  remote  from  the  injury,  so  that  it  cannot  be  caused 
by  direct  extension  of  inflammation  from  the  wound.  After  the  acute 
stage  is  over,  the  tissues  about  the  affected  articulations  become  thick- 
ened, and  partial  ankylosis  results,  Avhich  may  ultimately  destroy  the 
mobility  of  the  joint.  The  bones  also  may  become  swollen  and  thick- 
ened after  injuries  of  nerve-trunks,  and  in  young  people  the  same 
bones  may,  at  a  later  period,  be  arrested  in  their  development.  In 
progressive  unilateral  atrophy  of  the  face  the  bones  participate,  to  some 
extent,  in  the  wasting. 

2.  Affrctions  of  Spinal  Origin. — Attention  has  been  directed  by 
Charcot  and  his  scholars  to  the  great  fre(j[uency  with  which  nutritive 
changes  occur  in  joints  in  spinal  diseases.  These  joint  affections  may 
be  divided  into  acute  or  subacute,  and  chronic  arthritis. 

The  acute  or  subacute  form  is  accompanied  hj  more  or  less  severe 
pain,  tumefaction,  and  redness,  just  as  occurs  in  acute  rheumatism. 
This  form  occurs  in  Pott's  curyature,  traumatic  lesions  of  the  cord, 
idiopathic  myelitis,  progressive  muscular  atrophy,  acute  and  chronic 
poliomyelitis,  and  disseminated  sclerosis. 

Chronic  arthritis  is  irenerallv  observed  in  association  with  locomotor 


ir,2  GENEEAL    SYMPTOMATOLOGY. 

•ifixia  Tl.e  knee,  liip,  shoulder,  and  elbow-joints  are  most  frequently 
'attacked,  although  the  fingers  and  toes  are  also  liable  to  be  affected. 
When  the  tarsal  bones  are  affected  a  characteristic  deformity  is  pro- 
duced which  is  named  the  tabetic  foot.  The  joint  disease  usually 
betrins  about  the  same  time  as  the  locomotor  incoordination,  and  its 
onset  is  accompanied  or  preceded  by  severe  paroxysms  of  lancinating 
pains.  The  symptoms  begin  suddenly  in  the  absence  of  any  apprecia- 
ble external  cause,  generally  witliout  pain  or  febrile  reaction,  and  the 
joint  may  be  enormously  swollen  within  twenty-four  hours  from  the  com- 
mencement. The  general  tumefaction  disappears  after  a  few  days,  but  a 
more  or  less  considerable  local  swelling  remains,  caused  by  the  accumu- 
lation of  serous  fluid  in  the  joint  and  the  periarticular  serous  bursa-. 
The  fluid,  however,  disappears  from  the  joint  in  a  few  weeks  from  the 
onset.  In  tlie  bimigyi  form  of  the  affection  the  joint  may  recover  com- 
pletely, but  in  the  inalignant  form  the  articular  surfaces  become  greatly 
altered  and  so  roughened  that  cracking  sounds  are  heard  on  movement. 
After  a  time  the  heads  of  the  bones  become  atrophied  and  worn,  the 
ligaments  become  relaxed,  and  the  surrounding  muscles  ai'e  so  much 
atrophied  and  enfeebled  that  spontaneous  laxations  may  occur. 

Fractures. — Spontaneous  fractures  occur  not  infrequently  in  the 
course  of  locomotor  ataxia.  The  period  of  fracture  is  generally  pre- 
ceded by  two  or  three  severe  paroxysms  of  lancinating  pains,  the  limb 
is  then  found  swollen  and  presenting  all  the  symptoms  of  osteo-perios- 
titis,  and  it  then  becomes  fractured  on  the  slightest  movement,  or  in 
the  absence  of  any  movement  or  external  cause.  The  femur  is  more 
frequently  fractured  than  any  other  bone,  the  seat  of  fracture  being 
generally  the  neck,  but  the  bones  of  the  leg,  arm,  foreai*m,  and  indeed 
almost  every  bone  in  the  limbs  and  trunk,  includinjr  those  of  the 
vertebral  column,  have  been  found  fractured.  The  spontaneous  fract- 
ures of  ataxics  often  reunite  very  readily  and  rapidly,  with  an  enormous 
formation  of  callus.  The  earthy  phosphates  are  diminished  in  the 
bones  which  undergo  spontaneous  fractures,  forming  sometimes  ordy 
sixty  instead  of  eighty  per  cent,  of  the  bone  as  in  health,  while  tlie 
fatty  constituents  are  enormously  increased  in  amount. 

3.  Osseous  Affections  of  Cerebral  Origin. — In  the  spastic  hemiplegia 
of  infoncy  the  bones  on  the  paralyzed  side  are  arrested  in  their  devel- 
opment, being  smaller  and  shorter  than  tlie  corresponding  Ijones  on  the 
opposite  side.  In  hemiplegic  patients  arthroi)athies  of  the  joints  of 
the  hand  and  foot  are  met  with  which  -are  like  the  acute  arthropathies 
of  spinal  origin.  The  affection  begins  with  a  slight  swelling  and  local 
increase  of  temperature,  either  witli  or  without  pain  in  the  joint,  and 
at  times  tumefaction   and   redness  are  so  marked  as  to  resemble  the 


AFFECTIONS    OF    THE    GLANDULAK    APPAEATUS.      158 

articular  affections  bf  acute  rheumatism.  The  sheaths  of  the  tendons 
are  sometimes  implicated  along  with  the  joints.  These  arthropathies 
occur,  as  a  rule,  simultaneously  with  late  rigidity,  although  it  may 
begin  a  few  days  after  the  attack  or  at  a  much  later  period. 

4.  Osseous  Lesions  in  the  Insane. — In  insane  patients  the  bones 
may  either  become  so  soft  that  they  yield  readily  to  pressure,  and  thus 
l)roduce  various  deformities,  or  so  fragile  that  they  are  liable  to  undergo 
spontaneous  fracture,  and  may  be  found  to  crumble  readily  under  the 
finger  and  thumb  after  death.  Out  of  100  post-mortem  inspections  of 
the  insane  made  by  Gudden,  evidences  of  fracture  were  found  in  16 
cases,  and  cliiefly  in  men  who  had  suffered  from  general  paralysis.  In 
three-fourths  of  these  cases  there  were  multiple  fractures ;  in  one  case 
as  many  as  14,  in  another  23,  and  in  another  36  fractures.  The 
morbid  changes  which  occur  in  the  bones  of  the  insane  are  closely 
related  to  those  observed  in  the  spontaneous  fractures  of  locomotor 
ataxia. 

5.  Trophic  Affections  of  the  Teeth. — The  teeth  are  not  very  liable 
to  undergo  changes  in  diseases  of  the  nervous  system.  They  have 
been  known  to  fall  out  after  an  attack  of  herpes  affecting  the  maxillary 
branches  of  the  fifth  nerve,  probably  more  from  necrosis  of  the  bone 
than  from  disease  of  the  teeth  themselves.  Attention  has,  in  recent 
years,  been  directed  to  the  fact  that  the  teeth  sometimes  fall  out  sud- 
denly in  the  course  of  locomotor  ataxia,  and  in  the  al^sence  of  pain  or 
caries  of  the  bone.  They  have  also  been  observed  to  fall  out  in  a  case 
of  sclerosis  in  patches. 

VI.  Nutritive  and  Secretory  Affections  of  the 
Glandular  Apparatus. 

1.    Cutaneous  Secretory  Disorders. 

Various  pathological  facts  appear  to  prove  the  existence  of  cutaneous 
secretory  nerve  fibres  independently  of  the  vaso-motor  nerves.  Dimi- 
nution or  absence  of  the  secretion  of  sweat  may  at  times  exist  side  by 
side  with  local  increase  of  temperature  and  redness,  indicating  vaso- 
motor paralysis;  and,  conversely,  the  secretion  may  be  increased  in 
amount  along  with  local  diminution  of  temperature  and  pallor  of  the 
surface,  indicating  vaso-motor  spasm.  Recent  experiments  show  that 
peripheral  irritation  of  a  divided  sciatic  nerve  in  animals  induces  an 
increased  secretion  of  sweat  in  the  paralyzed  part. 

The  cutaneous  secretory  neuroses  consist  of  excessive  sweating  or 
hi/peridrosis,    diminution    or    absence  of  secretion   or  anidrosis,   and 


151  GENERAL    SYMPTOMATOLOGY. 

qualitative  changes  which  may  be  grouped  under  the  name  o^ paridrosis. 
The  profuse  sweating  of  acute  disease,  that  which  results  from  the 
action  of  various  toxic  agents,  and  the  partial  sweats  which  occur  dur- 
ing hysterical  and  epileptoid  attacks,  are  doubtless  of  nervous  origin. 
StTu  more  striking  examples  are  to  be  found  in  the  unilateral  perspira- 
tions which  have  ))een  described  under  the  name  of  Iniperidrosis  uni- 
lateraUs.  This  affection  is  sometimes  limited  to  one-half  of  the  head, 
and  at  other  times  extends  to  the  arm  of  the  same  side,  or  even  extends 
over  one-half  of  the  body,  and  is  usually  associated  with  severe  nervous 
affections,  such  as  hemicrania,  Graves's  disease,  dialietes  mellitus,  tal)es 
dorsalis,  and  general  paralysis  of  the  insane.  It  is  probably  caused  by 
lesion  of  the  sympathetic  or  of  the  cerebro-spinal  centres,  with  which 
it  is  united. 

Anidrosis  is  a  symptom  of  fever,  diabetes  mellitus,  chronic  13right"s 
disease,  and  of  certain  skin  diseases,  and  is  often  associated  with  grave 
nervous  diseases  like  general  paralysis  of  the  insane.  The  diminution 
of  ])erspiration  caused  by  various  toxic  agents  like  atropine  is  evidently 
due  to  action  on  the  nervous  system.  A  good  example  of  local  dryness 
of  the  skin  occurs  in  unilateral  atrophy  of  the  face,  an<l  a  similar  local 
condition  may  also  be  found  on  the  extremities  in  the  course  of  most 
of  the  different  cerebral,  spinal,  and  ])eripheral  chronic  nervous  affections. 

Paridroscs  of  various  kinds  have  been  observed  in  diseases  of  the 
nervous  system.  In  some  nervous  affections  the  secretion  emits  a 
peculiar,  generally  very  offensive,  odor — nsmidrosis.  S.  Weir  Mitchell 
observed  excessive  sweating,  Avith  stronjr  odor  of  vinegar,  after  severe 
contusion  of  peripheral  nerves,  and  in  one  case  the  smell  resembled 
that  of  a  bad  drain.  The  secretion  at  other  times  becomes  changed  to 
a  black,  blue,  red,  or  green  color,  chromidrosiH.  Colored  ])erspiration 
generally  occurs  in  hypochondriacs,  in  women  with  uterine  disorders 
of  various  kinds,  or  as  the  result  of  severe  emotional  disturbance.  In 
some  few  cases  extravasation  of  blood  takes  place  into  the  sweat  glands, 
giving  rise  to  bloody  sweating  or  Jicematidrosis.  This  condition  ajjpears 
to  be  occasionally  vicarious  menstruation,  but  it  is  usually  associated 
with  hysteria  and  other  central  nervous  affections.  It  is  probable  that 
in  most  of  the  cases  described  as  ha^matidrosis  the  coloring  matter  of 
the  blood  alone  escapes. 

2.  Secretory  Disorders  of  the  Salivary  G-Iands. 

Secretory  disorders  of  the  salivary  glands  may  occur,  in  connection 
with  lesions  of  the  peripheral  fibres  of  the  trigeminus,  the  facial  nerve, 
or  the  cervical  sympathetic.     An  increased  secretion  of  saliva  is  not 


AFFECTIONS    OF    THE    GLANDULAK    APPAEATUS.      155 

an  unusual  symptom  of  trigeminal  neuralgia,  caused  by  irritation  of  the 
lingual  branch  of  the  fifth  as  the  afferent,  and  the  chorda  tympani  as 
the  efferent  channel.  Stimulation  of  the  glosso-pharyngeal  nerve  also 
causes  an  increased  flow  of  saliva.  In  peripheral  paralysis  of  the 
facial  nerve,  caused  by  lesion  of  the  nerve  in  the  Fallopian  canal,  where 
it  is  accompanied  by  the  chorda  tympani,  the  secretion  of  saliva  is 
deficient  on  the  paralyzed  side,  because  the  secretory  fibres  of  the  sul)- 
maxillary  and  sublingual  glands  pass  through  the  chorda  tympani.  In 
paralysis  of  the  cervical  sympathetic  the  salivary  secretion  is  diminished 
in  quantity  because  tlie  ])arotid  gland  receives  a  portion  of  its  secretory 
fibres  through  the  cervical  sympathetic.  Irritation  of  the  sensory 
nerves  of  the  stomach,  especially  great  acidity  of  the  gastric  secretions, 
causes  an  increased  flow  of  saliva,  which  appears  to  be  an  automatic 
action,  by  means  of  Avhich  the  gastric  acidity  becomes  neutralized. 
Certain  poisons,  like  atropine,  paralyze  the  secretory  fibres  of  the 
chorda  tympani,  and  lead  to  a  diminution  or  arrest  of  the  salivary 
secretion :  whilst  others,  like  digitalis,  physostigmin,  nicotin,  and 
jaborandi,  irritate  the  secretory  fibres  and  cause  an  increased  flow  of 
saliva.  The  secretion  of  saliva  may  be  influenced  by  direct  or  reflex 
action  on  the  intracerebral  secretory  paths.  Bernard  found  that  an 
increased  flow  of  saliva  is  produced  by  ])uncture  of  the  floor  of  the 
fourth  ventricle  behind  the  origin  of  the  trigeminus,  and  it  is  probable 
that  the  increased  flow  of  saliA  a  observed  in  bulbar  paralysis  may  at 
times  be  due  to  irritation  of  this  point.  An  enormously  increased  flow 
of  saliva  has  been  observed  by  Eulenburg  in  dogs,  after  destruction  by 
the  actual  cautery  of  portions  of  the  cortex  of  the  brain  lying  in  front 
of  the  cruciate  sulcus.  The  saliva  flowed  out  in  a  constant  stream  from 
the  angle  of  the  mouth  on  the  opposite  side  to  the  injured  hemisphere, 
and  was  of  the  same  thin  watery  character  which  is  observed  after 
irritation  of  the  chorda  tympani. 

3.  Secretory  Disorders  of  the  Lachrymal  G-lands. 

Trio-eminal  neuralgia  gives  rise  to  an  increase  in  the  amount  of 
lachrymal  secretion  both  by  reflex  and  direct  action,  the  secretory  fibres 
of  this  gland  being  contained  partly  in  the  lachrymal  and  partly  in  the 
subcutaneous  malar  nerve.  After  traumatic  injury  of  the  cervical 
sympathetic  there  is  an  increased  flow  of  tears  on  the  affected  side, 
probably  from  vaso-motor  paralysis,  and  the  free  flow  of  tears  which 
often  takes  place  towards  the  termination  of  an  attack  of  hemicrania  is 
probably  caused  by  a  similar  mechanism.  Many  anomalies  in  the  flow 
of  the  lachrymal  secretion  are  doubtless  of  central  origin,  such  as  the 


15(3  GENERAL    SYMPTOMATOLOGY. 

copious  fl(jw  Avhich  occurs  in  hysterical  attacks  ami  in  connection  with 
emotional  disturbances. 

4.  Secretory  Disorders  of  the  Crlands  of  the  Digestive  Tract. 

An  increase  in  the  flow  of  the  secretions  of  the  stomach  and  intes- 
tines appears  to  be  caused  by  affections  of  the  vagus,  or  of  the  sympa- 
thetic plexuses  and  ganglia.  Diarrhoea  and  vomiting  are  often  caused 
by  emotional  disturbance,  and  they  may  also  accompany  hysterical 
attacks,  Avliile  apepsia  and  constipation  are  frequent  accompaniments  of 
numerous  cerebral  diseases.  Paroxysms  of  vomiting,  and  less  fre- 
([uently  of  diarrhoea,  are  also  prominent  symptoms  of  locomotor  ataxia. 

5.  Secretory  Disorders  of  the  GUnds  of  the  Crcnito-urinary  Apparatus. 

The  influence  of  the  nervous  system  on  the  secretion  of  urine  is  very 
great,  but  the  various  channels  by  means  of  which  it  is  conveyed  are 
not  accurately  ascertained.  The  most  notable  examples  are  polyuria 
and  diabetes  mellitus.  Various  anomalies  may  occur  in  the  secretions 
of  the  vagina,  uterus,  and  mannn?e  in  hysterical  females,  although  it 
is  doubtful  whether  they  are  due  to  affections  of  vaso-motor  or  secretory 
nerves.  In  tlie  condition  known  as  irritable  uterus  there  are  often,  in 
addition  to  the  sensory  disturbance,  numerous  anomalies  of  circulation 
and  secretion,  which  are  probably  of  reflex  origin.  Similar  phenomena 
may  be  associated  with  ilio-lumbar  neuralgia.  Attacks  of  hysteria  are 
often  followed  by  an  abundant  secretion  of  mucus  from  the  vagina,  and 
erotic  thoughts  may  give  rise  to  an  obstinate  discharge  in  the  absence 
of  any  organic  lesion.  In  "irritable  testis"  the  organ  and  the  sper- 
matic cord  are  often  swollen,  and  many  cases  of  spernuit«nThcea,  pollu- 
tions, and  aspermatism  may  probably  be  caused  by  functional  disturb- 
ances of  secretory  or  motor  nerve  fibres  issuing  from  the  lumbar  portion 
of  the  spinal  cord.  Pollutions  may  be  caused  by  reflex  irritation,  or 
by  an  increased  excitability  of  the  centre  of  ejaculation  in  the  spinal 
cord  in  such  diseases  as  tabes  dorsalis,  while  spermatorrhoea  is  caused 
most  probably  by  debility  of  the  vesiculse  seminales, 

VII.  Nutritive  Affections  of  the  Viscera 
(Visceral  Trophoneuroses), 

It  has  not  been  found  possible  to  separate  the  vaso-motor  and  trophic 
fibres  of  the  viscera,  either  with  regard  to  their  anatomical  distribution 
or  their  fiinctions.     It  is  very  likely  that  the  congestion,  ecchymoses, 


NUTRITIVE    AFFECTIONS    OF    THE    VISCEEA.  157 

and  extravasations  which  occur  in  various  central  nervous  diseases  are 
caused  '»y  implication  of  vaso-motor  nerves.  Cerebral  hemorrhage  is 
frequently  accompanied  by  i)ulmonary  apoplexy  or  pneumonia  of  the 
lung  on  the  side  opi)osite  to  the  lesion  ;  while  lesions  of  the  nuclei  of 
the  origin  of  the  pneumogastric,  or  of  tlie  nerve  itself,  may  give  rise 
to  pneumonia  and  fatty  degeneration  of  the  heart.  The  most  frequent 
consequences  of  extirpation  of  the  cteliac  and  mesenteric  plexuses  in 
animals  are  congestion  of  the  liver,  congestion  and  extravasations  in 
the  stomach  and  intestines,  and  diabetes — all  of  them  symptoms  wliicli 
are  likely  to  be  caused  by  vaso-motor  paralvsis. 


CHAPTER  YI. 

GENERAL  SYMPTOMATOLOGY  [continued). 

C.  THE  ELEMENTAKY  KINESIONEUROSES. 

The  movements  of  the  body  and  of  its  different  parts  are  caused  by 
muscular  contractions,  the  muscle  being  stimulated  to  act  by  impulses 
received  through  the  nervous  system,  when  a  nervous  stimulus  gives 
rise  to  a  muscular  contraction.  Elementary  motor  disorders  admit  of 
a  double  classification — the  one  anatomical,  the  other  physiological,  the 
two  traversing  each  other  at  right  angles. 

Anatomical  Classificatio7i. — Elementary  motor  disorders  may  be 
divided  into  those  which  affect  (i)  the  muscles  of  external  relation — 
the  external  Jcine8ioneuro.^es,  (ii)  the  muscles  of  the  internal  organs — 
internal  or  visceral  kinesioncuroses,  and  (ill)  the  muscular  fibres  of 
the  vascular  system — the  vascular  kincsicmcuroses,  or  the  angioncuroscs. 

Physiological  Classification. — Motor  disorders  may  be  divided  into 
(1)  the  conditions  in  which  there  are  excessive  muscular  contractions — 
spasms  or  hyperkineses,  (2)  those  conditions  in  Avliich  there  is  a  dimi- 
nution or  loss  of  the  power  of  exciting  the  muscles  to  contraction — 
paralyses  or  akineses,  and  (3)  various  anomalous  muscular  contractions 
which  may  be  comprised  under  the  name  of  the  synkineses.  The 
hyperkineses  and  akineses  may  be  subdivided,  according  to  the  func- 
tion of  the  nervous  apparatus  which  is  the  seat  of  the  lesion,  into  three 
classes,  namely :  a,  the  voluntary,  6,  the  reflex,  and  c,  the  automatic 
kinesioneuroses. 

I.  The  External  Kinesioneuroses. 

Methods  of  Examining  the  Motor  Apparatus. 

As  an  introduction  to  this  part  of  the  subject  it  will  be  useful  to 
describe  briefly  the  various  methods  employed  for  discovering  the  pres- 
ence or  absence  of  motor  disorders  of  the  external  muscular  apjiaratus. 
The  striped  muscles  are,  for  the  most  part,  connected  with  the  skeleton, 
and  by  their  contractions  they  move  the  bones  to  which  they  are 
attached,  and  thus  constitute  the  active  agents  in  maintaining  tlie 
various  attitudes  of  the  body.     The  graceful  form  of  the  body  is  also 


THE    EXTERNAL    KINESIONEU  ROSES.  159 

in  great  measure  due  to  the  rounded  bellies  of  the  muscles  which  help' 
to  fill  up  the  si)ace  between  the  bones  and  the  skin  and  the  subcutane- 
ous tissues.  In  subjecting  the  neuro-muscular  mechanism  of  external 
relation,  therefore,  to  a  methodical  examination  we  must  attend  (1) 
to  the  form  of  the  body  during  repose,  and  (2)  to  the  attitudes  of  the 
body  during  actual  or  attempted  movements. 

1.  Examination  of  the  Body  during  Repose. 

The  1)ulk  and  consistence  of  a  muscle  as  felt  through  the  skin  may, 
as  a  rule,  l)e  accepted  as  a  more  or  less  adequate  sign  of  the  degree  of 
its  nutrition  and  motor  power,  and  consequently  an  examination  of  the 
exposed  body  by  inspection  and  palpation  affords  much  valuable  in- 
formation with  regard  to  the  motor  mechanism.  If,  for  instance,  the 
outer  surface  of  the  shoulder  is  seen  to  be  flattened  and  the  head  of 
the  humerus  can  l)e  felt  immediately  underlying  the  skin,  it  is  known 
that  the  deltoid  is  wasted,  and  if  the  opposite  shoulder  is  at  the  same 
time  plump  and  rounded,  it  is  inferred  that  the  deltoid  of  the  affected 
shoulder  is  Avasted  from  a  special  and  not  from  a  general  cause.  But 
if  the  deltoid,  instead  of  being  wasted,  is  unduly  prominent  and  tense, 
and  the  elbow  is  held  })ermanently  removed  from  the  trunk,  it  is  at 
once  a])parent  that  the  muscle  is  the  subject  of  spasm.  Distortion  of 
the  limbs  often  shows  at  once  that  certain  groups  of  muscles  must  be 
paralyzed,  or  that  their  antagonists  are  in  a  state  of  spasm,  and  pei'- 
formance  of  passive  movements  will  generally  decide  this  question, 
showing  directly  whether  a  particular  group  of  muscles  is  relaxed  or 
tense.  In  the  case  of  spasm  valuable  information  may  be  obtained  by 
producing  a  corresponding  deformity  on  the  healthy  side  by  means  of 
the  faradic  current,  and  in  the  case  of  paralysis,  by  exciting  the 
antagonists  of  the  affected  muscles  to  contraction  by  means  of  fara- 
dization. 

2.  Examination  of  the  Body  during  Movement. 

The  muscles  of  external  relation  may  be  excited  to  contraction  by 
(a)  voluntary,  (b)  reflex,  (c)  automatic,  (d)  mechanical,  and  (e)  electrical 
stimuli,  and  the  response  of  the  muscles  to  one  or  more  of  these  stimuli 
may  be  wanting,  excessive,  or  otherwise  disordered. 

(a)  Voluntary  Movements. — The  student  should  make  a  careful 
study  of  the  different  forms  of  disordered  locomotion,  and  be  able  to 
distinguish  at  a  glance  the  hemiplegic  walk,  the  spastic  gait,  and  the 
loose  and  dangling  limbs  of  the  various  forms  of  atrophic  paralysis. 
The  patient  should  be  asked  to  perform  special  movements,  such  as 
standing  on    one    leg,  standing  with  feet  touching  along  their  inner 


1(50  GENERAL    SYMPTOMATOLOGY. 

1  .orders  (tlic  eyes  being  closed),  ascending  a  stair,  writing,  speaking, 
and  mimetic  facial  movements,  in  order  that  any  deviation  from  the 
normal  may  be  carefully  observed.  Attention  should  be  directed  to 
ascertain  whether  incapacity  to  perform  a  particular  movement  is  caused 
bv  ])aralysis  of  a  group  of  muscles  or  spasm  of  their  antagonists.  An 
approxiiiiate  estimate  can  be  formed  of  the  degree  of  paralysis  present 
by  comparative  testing  of  the  resistance  which  can  be  opposed  by  i)as- 
sive  movements,  while  a  more  accurate  test  of  motor  power  which 
can  be  increased  by  certain  groups  of  muscles  is  afforded  by  the  various 
forms  of  dynamometers.  It  is  also  important  to  observe  whether  the 
muscular  contraction  can  be  maintained  for  some  time  without  inducing 
exhaustion,  and  whether  the  intended  movement  is  executed  with  pre- 
cision and  steadiness,  or  is  interrupted  by  tremors  and  antagonistic 
secondary  movements.  Slowness  in  executing  certain  movements  is  a 
sign  of  diminished  motor  i)Ower,  and  feebleness  of  the  muscles  of  the 
liaiid,  for  instance,  may  sometimes  be  more  readily  detected  by  asking 
the  patient  to  write  his  name  or  to  perform  the  "  devil's  tattoo  "  on  the 
tal)le,  than  by  estimating  the  strength  of  the  grasp. 

(b)  Heflex  movements  may  be  tested  by  tickling,  pricking,  pinching, 
and  faradic  excitation  of  the  skin  and  accessible  mucous  meml.ranes. 
The  reflexes  of  the  special  senses  nnist  be  tested  by  their  special  exci- 
tants, while  it  is  most  important  to  examine  the  deep  reflexes  by  ta])- 
ping  tendons,  fascige,  and  the  periosteum. 

(c)  Automatic  Movements. — The  movements  of  respiration  and  of 
the  iris,  and  the  action  of  the  sphincters,  may  be  mentioned  as  examples 
of  automatic  actions  which  ought  to  be  carefully  observed.  In  ordinary 
locomotion,  the  observer  ought  to  be  able  to  distinguish  at  a  glance  the 
ataxic  walk,  the  cerebellar  reel,  the  staggerinir  gait  of  ^Meniere's  disease, 
and  the  uncertain,  tremulous  walk  of  sclerosis  in  patches. 

(d)  Mechanical  Stimuli. — A  moderately  strong  blow  over  almost 
any  muscle  induces  a  contraction  of  the  fasciculus  struck,  especially  if 
the  blow  fall  near  the  point  of  entrance  of  the  motor  nerves.  In  ex- 
hausting diseases  like  phthisis,  when  the  nutrition  of  the  muscles  is 
greatly  diminished,  a  sharp  blow  causes  the  formation  of  a  wheal  which 
lasts  several  seconds,  and  from  which  small  waves  of  contraction  run  in 
l)oth  directions  towards  the  extremities  of  the  muscle,  this  reaction 
l)eing  called  idio-muscular  contraction. 

(e)  Electrical  Stimuli.~T\\e  electrical  currents  usually  employed  for 
clinical  investigation  are  (1)  the  faradic  and  (2)  the  galvanic  currents. 

(1)  The  faradic  current  consists  of  a  series  of  isolated  currents,  each 
of  momentary  duration,  and  of  very  rapid  development  and  decline, 
following  each  other   in   (piick  succession   and  flowing  alternately  in 


THE    EXTEEXAL    KIXESIONEU  ROSES .  161 

oi)posite  directions.  Faradic  exeitahility  or  irritability  is  tlie  term 
used  to  designate  the  kind  and  strength  of  the  reactions  exhibited  hy 
muscles  and  nerves  under  the  influence  of  the  faradic  current.  Mus- 
cuLir  contraction  may  be  induced  by  the  direct  application  of  the  faradic 
current  to  the  muscles  themselves,  or  indirectly  through  excitation  of 
the  motor  nerves.  The  cathode  of  the  secondary  induced  current  is 
usually  employed  as  the  exciting  pole,  while  the  anode  may  be  placed 
upon  some  indifferent  part  of  the  body,  as  the  sternum  or  patella. 
Direct  excitation  of  accessible  muscles  is  best  performed  when  the  poles 
are  applied  over  the  points  at  which  the  motor  nerves  enter  the  muscles, 
which  may  be  ascertained  by  reference  to  Ziemssens  diagrams.  The 
faradic  excitability  of  both  nerves  and  muscles  in  diseased  conditions 
admits  only  of  quantitative  changes.  It  may  remain  normal  or  be 
slightly  increased  in  cases  of  muscular  spasm,  in  that  form  of  muscular 
paralysis  which  is  attended  by  tension,  and  in  hysterical  pai-alysis ; 
while  it  is  diminished  or  lost  in  that  form  of  paralysis  which  is  attended 
by  wasting  of  the  muscles,  with  the  exception  of  the  active  stage  of 
progressive  muscular  atrophy,  in  which  it  may  be  increased.  The 
degree  of  the  excitability  runs  a  more  or  less  parallel  course  in  the 
nerves  and  muscles. 

(2)  The  galvanic  current  is  continuously  produced  and  runs  in  the 
same  direction,  and  with  the  same  intensity,  but  by  means  of  the  com- 
mutator the  current  may  be  interrupted  at  pleasure,  or  even  quickly 
reversed,  a  change  which  induces  a  very  powerful  contraction. 

G-alvanic  excitability  or  irritability  is  a  term  used  to  express  the 
reactions  obtained  in  response  to  opening  and  closing  the  circuit,  and 
to  the  continuous  passage  of  the  current.  The  law  of  contraction 
both  of  motor  nerves  and  muscles  rests  upon  the  facts  that  the  cathode 
produces  contraction  chiefly  on  closure  of  the  current,  the  anode  chiefly 
on  opening  the  current,  and  that  the  stimulus  of  the  cathode  is  stronger 
than  that  of  the  anode. 

The  law  of  normal  contraction  may  be  expressed  by  the  following 
formulae. 

Let  An  =  anode,  Ca  =  cathode,  C  =^  medium  contraction,  c  = 
feeble  contraction,  C  =  strong  contraction,  S  =^  closure  of  current, 
0  =  opening  of  current,  Te  =  tetanic  contraction,  thus: 

Weak  currents  produce  CaSc. 

Medium  currents  produce  CaSC,  AnSc,  AnOc. 

Strong  currents  produce  CaSTe,  AnSC,  AnOC,  CaOc. 

In  diseased  conditions  the  law  of  contraction  may  remain  (a)  normal, 
or  deviations  from  the  normal  law  may  occur  by  way  of  {h)  increase  or 

11 


1^2  GENERAL    SYMPTOMATOLOGY. 

{c)  diminution  of  the  excitability,  or  by  changes  in  (d)  the  quality  of 
the  various  reactions. 

(a)  A  normal  degree  of  the  galvanic  excitability  is  obtained  in  cases 
of  muscular  spasm,  in  hysterical  paralysis,  and  in  paralysis  attended 
by  muscular  tension. 

(h)  Simple  increase  of  the  galvanic  excitability  occurs  in  certain 
forms  of  spasmodic  paralysis,  tabes  dorsalis,  and  as  a  transient  symptom 
in  a  few  cases  of  peripheral  paralysis.  Increase  of  the  excitability 
gives  rise  to  the  following  deviations  from  the  normal  law  : 

Weak  currents  produce  CaSC,  AnOC. 

Medium  currents  produce  CaSTe,  AnOC,  CaOC. 

Strong  currents  produce  CaSTe,  AnOTe,  CaOC. 

(c)  Simple  diminution  of  the  galvanic  excitability  occurs  in  all  those 
cases  in  which  paralyzed  muscles  undergo  a  minor  degree  of  atrophy. 
The  following  formulae  express  simple  diminution  of  excitability  : 

First  degree,  strong  currents  produce  CaSC,  AnSc,  AnOc. 
Second  degree,  strong  currents  produce  CaSc. 

(d)  Qualitative  as  ivell  as  quantitative  alterations  of  the  excitability 
are  found  in  all  those  cases  in  which  paralyzed  muscles  undergo  a  con- 
siderable or  a  profound  degree  of  atropliy,  and  this  kind  of  reaction 
has  consequently  been  called  the  "atrophic  test,"  or  the  "reaction  of 
deo-eneration."  The  alterations  in  the  reaction  of  the  nerves  and  the 
muscles  do  not  run  a  parallel  course,  so  that  the  two  must  be  separately 
described. 

(j)  Reaction  of  the  Affected  Nerves. — The  reaction  in  the  afiected 
nerves  begins  on  the  second  and  third  day  after  a  severe  attack  of  that 
form  of  paralysis  which  will  be  subsequently  described  as  atrophic 
paralysis,  and  a  continuous  uniform  diminution  of  the  galvanic  as  of 
the  faradic  excitability  is  observable  without  any  qualitative  change,  and 
in  rare  cases  only  is  it  preceded  by  slight  increase.  The  diminution 
begins  in  the  part  nearest  the  lesion,  and  extends  rapidly  to  the 
periphery.  At  the  end  of  the  first,  or  in  the  course  of  the  second 
week  (from  the  seventh  to  the  twelfth  day),  the  excitability  wholly  dis- 
appears. In  incurable  cases  the  loss  of  the  excitability  is  permanent, 
but  if  repair  of  the  diseased  tissue  takes  place,  the  excitability,  after 
being  lost  for  a  variable  period,  is  restored.  The  reactions  to  both  cur- 
rents appear  simultaneously,  beginning  first  in  the  central  segments  of 
the  nerve  and  spreading  slowly  to  the  periphery. 

(jj)  Reaction  of  the  Affected  3Iuscles. — The  reactions  obtained  by 
the  application  of  the  faradic  current  directly  to  the  muscles  are 
quite  similar  to  those  obtained  from  the  application  of  the  current  to 
the  degenerated  nerves.     When  the  electrode  is  placed  over  the  para- 


THE    EXTERNAL    KINESIONEUROSES.  163 

Ivzed  muscle  a  diminution  of  the  excitability  is  observed  to\^ards  the 
end  of  the  first  week,  and  in  severe  cases  there  is  complete  extinction 
of  it  towards  the  end  of  the  second  week.  When  the  case  is  incurable 
the  foradic  contractility  of  the  muscle  is  permanently  abolished,  but  in 
curable  cases  it  reappears  along  with  the  restitution  of  voluntary  power, 
although  usually  somewhat  later  than  in  the  nerves.  As  recovery  pro- 
ceeds the  faradic  excitability  increases  gradually  but  slowly,  and  o-en- 
erally  remains  for  a  long  time  abnormally  low,  especially  if  the  paralysis 
has  been  of  long  duration. 

The  galvanic  excitabiUf//  falls  slightly  during  the  first  week,  but  in  the 
course  of  the  second  week  it  becomes  enormously  increased  and  con- 
tinues to  increase  until  about  the  end  of  the  fourth  week.  The  aifected 
muscles  now  respond  to  currents  much  too  feeble  to  act  upon  healthy 
muscles.  The  character  of  the  contractions  is  also  changed,  and 
instead  of  appearing  suddenly  and  being  of  short  duration,  as  in 
health,  they  now  develop  gradually  and  slowly,  are  protracted  in  dura- 
tion, and  readily  pass  into  tetanus  even  when  produced  by  feeble 
currents. 

The  law  of  muscular  contraction  also  becomes  qualitatively  altered,  so 
that  anodal  closing  contraction  soon  equals  or  exceeds  cathodal  closing 
contraction  (AnSC  =  or>  CaSC),  and  cathodal  opening  contraction  soon 
equals  or  exceeds  anodal  opening  contraction  (CaOC  =  or  >  AnOC). 
The  following  formulge  express  the  qualitative  changes  in  the  reaction 
of  degeneration: 

Weak  currents  produce  during  stage  of  increase  CaSC,  AnSTe, 
AnOC,  CaOC. 

^ledium  currents  produce  during  stage  of  gradual  decrease  CaSc, 
AnSTe. 

Strong  currents  produce  during  final  stage  prior  to  abolition  AnSc. 

The  following  diagrams,  borrowed  from  Erb,  represent  graphically 
the  general  relations  of  motor  power,  electrical  excitability  and  struct- 
ural changes  of  the  nerves  and  muscles  which  are  present  in  the  differ- 
ent stages  of  paralysis.  The  first  tliick  vertical  line  or  ordinate  indi- 
cates the  sudden  appearance  of  paralysis  ( IBD )»  and  the  period  of 
return  of  motor  power  is  indicated  by  a  (  *  ),  whilst  the  succeeding 
ordinates  represent  intervals  of  one  or  more  weeks  dating  from  the 
occurrence  of  the  attack.  The  undulations  in  the  line  representing 
the  galvanic  excitability  of  the  muscles  indicate  qualitative  changes  in 
the  reactions.  In  the  first  degree  of  the  reaction  of  degeneration 
(Fig.  66),  the  electrical  excitability  of  both  nerve  and  muscle  falls 
during  the  first  week,  the  nerves  lose  all  their  electrical  reactions 
during  the  second  week,  but  the  muscles  lose  only  their  faradic  con- 


164 


GENERAL    SYMPTOMATOLOGY 


tractility  during  tliis  period,  wliilst  the  galvanic  excitability  becomes 
greatly  increased  and  manifests  the  qualitative  changes  already  de- 
scribed.    At  the  end  of  the  sixth  week  there  is  a  gradual  return  of 


Degeneration 
of  the  Nerve. 


Fig.  06. 
Recovery  Rapid. 
Atrophy  and 
Multiplication  of  Nuclei 
in  the  Blusciilar  Fibres 


Regeneration 


Motility. 

i  (  Galv. 

I  1  Farad. 

g  ("Galv.      and 
tj  -;  Farad.  Excit- 
|z;  (ability. 


10.      U       12.       Week. 


motor  power,  and  at  the  end  of  the  seventh  week  there  is  a  gradual 
return  of  the  electrical  reactions  of  the  ner\'e  and  of  the  faradic  con- 
tractility of  the  muscle,  while  the  galvanic  reactions  of  the  muscle 
gradually  sink,  and  the  (iualitati\e  changes  disaj)pear  until  gradually 
the  normal  reaction  is  established. 

In  ''the  second  degree  of  the    reaction  of  degeneration   the   faradic 


Degeneration 
of  the  Nerve. 


FlO.  67. 
Recovery  Slow 
Atrophy,  etc  , 

of  jrviscles. 


]{egeneration. 


1.     2.      4.      i;.      111.    15.    20.    2.'>.    :?(i 


Motility. 

Galv. 

Farad. 


g  ( Galv.      and 
•g  •<  Farad.  Excit- 
>5  (ability. 


and  galvanic  excitability  of  the  nerve  does  not  appear  until  the  thirtieth 
week  (Fig.  67),  while  in  the  third  degree  (Fig.  68)  the  excitability  of 
the  nerve  never  returns,  but  the  galvanic  excitability  of  the  muscle 


THE    EXTERNAL    KINESIONEUROSES. 


165 


only  becomes  finally  lost  after  a  pi-olonged  period,  in  some  cases  extend- 
ing over  a  period  of  two  years. 

A  "partial  reaction  of  degeneration"  (Fig.  69)  has  been  described 
by  Erb,  in  which  the  faradic  and  galvanic  excitability  of  the  aifected 


4  \  Galv. 

^  (  Farad. 

=■  (Galv.      and 
^  -  Farad.  Excit- 
5^   (ability. 


Degeneration 
of  the  Nerve. 


Fig.  (58. 

No  Recovery. 

Atropliy, 
Jlultiplication  of  Nuclei,  Cirrhosis 


t'omplete 
Disappearance. 


1        3.      1(1.     211. 


o.     80.     till.     1(1(1.     Week. 


nerve  is  diminished,  but  not  abolished,  the  diminution  beino-  sometimes 
only  to  a  slight  degree.  The  faradic  excitability  of  the  paralyzed 
muscle  undergoes  a  diminution  corresponding  to  that  of  the  nerve,  but 
the  galvanic  excitability  of  the  muscles  manifests  the  quantitative  and 
([ualitative  changes  which  are  so  characteristic  of  the  severer  form  of 
the  reaction  of  degeneration. 

Fig.  G9. 


Atrophy  and 
Degeneration  of        Multiplication  of  Nuclei 
the  Nerve  (?)  in  the  Muscular  Fibres. 


KeKeneratiou 


Motility. 

1 

fGalv. 
(Farad. 

(Galv. 
^  Farad, 
(ability. 

and 
Excit 

1.  Hypcrkinesis  of  the  3Iuscles  of  External  Relation. 

Hyperkinesis  of  the  voluntary  muscles  consists  of  abnormal  contrac- 
tions called  spasms.     Muscular  spasms  consist  of  contractions  which 


IQQ  GENERAL    SYMPTOMATOLOGY. 

are  disproportionate  to  the  degree  of  external  stimulus,  or  which  arise 
in  the  absence  of  external  stimulation  as  the  result  of  morbid  irritation. 
Spasmodic  affections  may  be  divided  into,  a,  clonic  spasms,  in  which 
the  muscles  are  in  a  state  of  rapidly  alternating  contractions  and  re- 
laxations ;  and,  b,  tonic  spasms,  in  which  the  affected  muscles  are 
maintained  in  a  state  of  persistent  and  equable  contraction. 

a.  Clonic  Spasms. 

(1)  Tremor  is  the  mildest  form  of  clonic  spasm.  It  consists  of  slight 
contractions  of  groups  of  muscles  by  means  of  which  a  peculiar 
rhythmical  oscillation  of  the  limbs  and  trunk  is  produced.  The  higher 
degrees  of  tremor  cause  manifest  trembling  of  the  limbs  and  trunk, 
while  fibrillary  contractions  consist  of  alternate  contractions  and  re- 
laxations of  individual  bundles  of  muscular  fibres  which  are  visible  as 
wavy  oscillations  under  the  skin,  but  do  not  give  rise  to  any  movement 
of  the  limb.  There  are  two  chief  varieties  of  the  severer  form  of 
tremor  which  moves  the  limbs :  one  of  which  persists  during  repose, 
and  is  met  Avith  in  paralysis  agitans ;  and  the  other  which  appears  only 
when  the  patient  makes  a  voluntary  effort,  and  is  observed  in  sclerosis 
in  patches, 

(2)  Convulsion  is  the  severest  form  of  clonic  spasm.  It  consists  of 
energetic  contractions  and  relaxations  of  particular  muscles  or  groups 
of  muscles  which  produce  a  rapid  succession  of  vigorous  movements, 
and  give  rise  to  twitchings  of  the  face,  startings  of  the  limbs,  and 
movements  of  the  head  and  body.  If  the  majority  of  the  muscles  of 
the  body  are  affected  with  alternating  contractions  and  relaxations,  so 
that  extensive  and  irregular  movements  of  the  trunk  and  limbs  are 
produced,  the  condition  is  termed  general  convulsion,  which  forms  the 
most  prominent  feature  of  epilepsy,  uraemia,  eclampsia,  and  hysterical 
attacks. 

h.  Tonic  Spasms. 

(1)  Cramp  is  the  simplest  form  of  tonic  spasm,  and  consists  of  a 
persistent  painful  contraction  of  a  muscle  or  of  a  group  of  muscles. 
Cramp  of  the  calf  is  the  most  common  variety  of  this  affection  when  it 
IS  limited  to  a  single  muscle,  while  tetanus  may  be  taken  as  the  best 
example  when  the  majority  of  the  muscles  of  the  body  are  affected. 

A  peculiar  modification  of  cramp  is  met  with  in"^  catalepsy.  The 
muscles  are  moderately  contracted,  but  the  resistance  they  "offer  to 
passive  movements  may  be  readily  overcome,  and  the  limbs  may  be 
made  to  assume  constrained  positions  which  thev  retain.     From  the 


THE    EXTERNAL    KINESION  EUROSES.  167 

manner  in  which  the  limbs  can  be  moulded  into  various  positions  this 
condition  has  been  caWed  Jiexibilitas  cerea. 

(2)  Muscular  tension  is  a  state  of  moderate  contraction  of  muscles 
which  occurs  either  when  they  are  stretched  by  passive  movements  or 
by  a  voluntary  contraction  of  their  antagonists.  This  condition  is 
always  associated  with  a  certain  degree  of  loss  of  voluntary  power  over 
the  affected  muscles. 

(3)  Contracture  is  meant  to  express  any  persistent  shortening  of  a 
muscle,  whereby  its  points  of  origin  and  insertion  are  permanently 
approximated.  The  varieties  of  contraction  are  myopatliic  contracture, 
when  the  shortening  occurs  as  a  result  of  disease  in  the  muscle  itself; 
imralytic  or  secondary  contracture,  when  it  occurs  in  healthy  muscles 
which  have  their  ends  permanently  approximated  owing  to  paralysis  of 
their  antagonists ;  and  primary  or  neuropathic  contracture,  when  the 
muscles  are  persistently  rigid  and  shortened  from  abnormal  innervation, 
a  condition  which  is  always  associated  with  a  certain  degree  of  paralysis. 
In  the  last  variety  the  rigidity  of  the  muscle  usually  disappears  during 
sleep  and  gradually  returns  on  awakening,  and  it  is  almost  always  in- 
creased by  voluntary  and  passive  movements. 

Pressure  points  are  frequently  observed  in  spasmodic  affections. 
Pressure  upon  certain  points  puts  a  stop  at  times  to  the  convulsion 
when  present,  and  consequently  these  points  may  be  called  pressure- 
arresting  points.  In  other  cases  the  convulsions  are  brought  on  by 
pressure  on  particular  points,  and  these  may,  therefore,  be  called  pres- 
sure-exciting points.  Pressure  points  of  the  first  kind  have  been  par- 
ticularly observed  in  facial  spasm,  and  they  correspond,  like  the  painful 
points  in  neuralgia,  to  the  various  branches  of  the  trigeminus,  and  are 
not  unfrequently  sensitive  to  pressure. 

Spasms  are  caused  by  increased  irritability  of  some  part  of  the  motor 
nervous  mechanism.  When  the  spasm,  Avhether  it  be  clonic  or  tonic, 
is  limited  to  the  area  of  distribution  of  particular  nerves,  the  lesion  is 
most  probably  situated  in  some  part  of  the  spino-neural  system,  either 
in  the  centre  or  efferent  fibre,  or  in  some  afferent  fibres,  the  last  con- 
stituting rejlex  spasms.  Paroxysmal  clonic  convulsions  are  caused  by 
irritation  of  the  cortex  of  the  brain,  and  certain  forms  of  tonic  and 
clonic  spasms  are  caused  by  irritation  of  the  fibres  of  the  pyramidal 
tracts.  Paroxysmal  tonic  contractions  are  most  probably  caused  by 
irritation  of  the  cortex  of  the  cerebellum.  Persistent  muscular  tension 
and  contracture  are  caused  by  disease  of  the  pyramidal  tracts,  and  are 
associated  with  paralysis.  Dr.  Hughlings  Jackson  explains  the  pres- 
ence of  tension  under  such  circumstances  by  supposing  that  the  with- 
drawal of  the   cerebral  influence  allows  the  tonic  action  of  the  cere- 


1(38  GENERAL    SYMPTOMATOLOGY. 

bellum  to  become  predominant.  Against  this  theory  it  is  urged  that 
tension  is  present  in  cases  of  transverse  myelitis,  in  Avhich  both  the 
cerebral  and  cerebellar  influences  are  withdrawn.  It  is  therefore  prob- 
able that  muscular  tension  is  caused  by  the  removal  of  the  inhibitory 
action  of  the  cerebrum,  owing  to  disease  of  the  pyramidal  tracts,  per- 
mission being  thus  given  for  the  predominant  action  of  the  reflex 
nervous  mechanisms  of  the  spinal  cord. 

2.  Akinesis  of  the  Muscles  of  External  Relation. 

By  akinesis  or  paralysis  of  the  muscles  of  external  relation  is  under- 
stood the  diminution  or  abolition  of  the  power  to  contract  the  affected 
muscles  by  voluntary  effort.  The  term  paresis  is  used  to  denote  tlie 
diminution  of  motor  power.  Some  authors  have  endeavored  to  restrict 
paralysis  to  its  complete  abolition,  but  this  term  Avill  be  employed  hei-e 
in  a  generic  sense  as  embracino;  both  conditions. 

Classification. 

Paralyses  of  the  muscles  of  external  relation  are  susceptible  of  being 
classified  according  to  the  nature,  cause,  and  situation  of  the  lesion,  the 
distribution  of  the  paralysis,  and  the  functional  disorders  of  the  muscles 
which  accompany  paralysis  of  them.  Tliese  divisions  constitute  the — 
I,  pathological,  ii,  etiological,  ill,  topographical,  iv,  clinical,  and,  v, 
physiological  classification. 


I.    THE  PATHOLOGICAL  CLASSIFICATION. 


The  diff'erent  varieties  of  paralysis  are  arranged,  according  to  the 
nature  of  the  lesion,  into  rheumatic,  syphilitic,  inflammatory,  and  other 
forms.  They  may  also  be  divided  into  organic  and  functional  lesions, 
according  as  the  morbid  changes  which  underlie  the  paralysis  are  or  are 
not  capable  of  being  recognized  by  our  present  means  of  research. 

II.    THE  ETIOLOGICAL  CLASSIFICATIOX. 

The  functional  paralyses  are  not  susceptible  of  being  arranged 
according  to  the  situation  of  the  lesion,  and  they  are  therefore  usually 
classified  according  to  tlie  cause  of  the  aff"ection.  They  are  usually 
divided  into  (1)  toxic,  (2)  febrile  and  post-febrile,  (3)  reflex,  (4)  post- 
epileptic, and  (5)  hysterical  paralysis. 

III.    THE  TOPOGRAPHICAL  CLASSIFICATION. 

The  organic  paralyses  lend  themselves  readily  to  a  classification 
according  to  the  situation  of  the  lesion.     They  may  be  divided  into  (i) 


THE    EXTERNAL    KINESIONEU  ROSES.  169 

myopathic  paralyses,  or  those  in  Avhicli  tlie  primary  disease  is  situated 
in  the  muscles  themselves,  and  (ii)  neuroiyathic  paralyses,  or  those  in 
Avhich  the  primary  disease  is  localized  in  some  part  of  the  nervous 
system. 

The  neuropathic  paralyses,  with  which  we  have  to  do  chiefly  here, 
may  be  subdivided  into  (1)  cerebral,  (2)  spinal,  and  (3)  neural  or 
peripheral  i)aralyses,  according  as  the  lesion  is  situated  in  the  brain, 
spinal  cord,  or  peripheral  nerves  respectively.  But  although  this  divi- 
sion is  very  convenient,  a  much  more  important  distinction  is  that  which 
divides  them  into  (1)  cerebrospinal  and  (2)  spino-neural  paralyses. 

In  the  cerebrospinal  variety  the  lesion  is  situated  either  in  the  motor 
centres  of  the  cortex  of  the  brain  or  in  the  pyramidal  tracts. 

In  the  spino-neural  variety  the  lesion  is  situated  in  the  anterior  gray 
horns  of  the  spinal  cord  and  their  upward  continuations  in  the  medulla 
oblongata,  pons,  and  crura  cerebri,  or  in  the  fibres  of  the  })eripheral 
nerves  which  connect  the  ganglion  cells  of  these  horns  with  the  muscles. 
It  will  immediately  be  found  that  this  topographical  division  corresponds 
more  or  less  closely  with  the  divisions  of  the  physiological  classification, 
and  this  constitutes  its  chief  advantage. 

It  may  here  be  noticed  that  when  the  lesion  is  restricted  to  one  of 
the  physiological  tracts  of  the  spinal  cord  the  affection  is  called  a 
system-disease,  and  when  several  of  them  are  simultaneously  implicated 
the  affection  is  called  a  mixed  or  indiscriminate  disease.  Amongst 
the  mixed  diseases  we  shall  also  include  complicated  cases  of  cerebral 
paralysis. 

IV.    THE  CLINICAL  CLASSIFICATION. 

Various  names  have  been  given  to  a  paralysis  according  to  its  extent 
and  distribution.  The  paralysis  is  sometimes  limited  to  a  single  muscle 
or  group  of  muscles,  or  all  the  muscles  supplied  by  a  single  nerve  or 
plexus  of  nerves  may  be  implicated  ;  when  all  or  almost  all  the  muscles 
of  a  single  extremity  are  paralyzed,  the  condition  is  called  a  monoplegia. 
In  other  cases  the  paralysis  afi'ects  both  halves  of  the  body  symmetri- 
cally, and  then  it  generally  begins  in  the  lower  extremities,  and  spreads 
to  the  trunk  and  upper  extremities.  This  is  the  usual  form  of  paralysis 
Avhich  results  from  disease  of  the  spinal  cord,  and  is  termed  paraplegia. 
In  other  cases  the  paralysis  afi'ects  the  lateral  half  of  the  body,  impli- 
catino;  the  face,  arm,  and  le<z  of  the  same  side,  and  it  is  then  termed 
hemiplegia.  The  lesion  which  causes  this  form  of  paralysis  is  usually 
situated  in  the  opposite  hemisphere  of  the  brain  ;  hemiplegia  of  spinal 
origin  is  named  hemiparaplegia.  When  the  upjier  and  lower  extremi- 
ties on  both  sides  are  paralyzed,  the  condition,  when  due  to  spinal  dis- 


170  GENEEAL    SYMPTOMATOLOGY. 

ease,  has  been  named  paraplegia  cervicalis,  and  when  caused  by  cerebral 
disease,  bilateral  hemij^legia,  or  pamplegia.  When  the  ocular  or  flicial 
muscles  on  one  side,  and  the  limbs  on  the  opposite  side,  are  paralyzed, 
the  condition  is  called  crossed  or  alternate  hemiplegia. 

V.    THE  PHYSIOLOGICAL  CLASSIFICATION. 

A  much  more  important  distinction  than  those  depending  upon  the 
extent  and  distribution  of  the  affection  is  that  which  divides  the  various 
forms  into  (1)  atrophic,  and  (2)  spastic  or  spasmodic  paralysis.  This 
division  does  not  embrace  every  form  of  paralysis,  inasmuch  as  in  some 
paralytic  affections  the  muscles  neither  undergo  active  Avasting,  nor  are 
affected  by  spasm.  This  distinction  is,  nevertheless,  a  very  important 
one,  and  ought  to  be  kept  in  view  in  the  clinical  examination  of  every 
case  of  paralysis.  Both  atrophic  and  spasmodic  paralyses  embrace 
some  forms  of  myopathic  paralysis,  but,  when  these  are  due  to  an 
organic  disease  of  some  part  of  the  nervous  system,  they  correspond 
respectively  to  the  spino-neural  and  cerebro-spinal  paralyses  of  the 
topographical  classification. 

The  different  methods  of  classification  are  combined  into  one  scheme 
in  the  following  tables  : 


THE    EXTERNAL    KINESIONEUROSES. 


171 


T-ABLE  I. — Hetiropathie  Paralyses. 


A.  ORGANIC  PARALYSES. 
,  Spino-neural  or  Atrophic  Paralyses. 

I.  Neural  or  Peripheral  Paralysis. 

II.  Reflex  Atrophic  Paralysis. 


1.  Acute  Atrophic  Spinal  Paralysis  of  Infants. 

2.  Acute  Atrophic  Spinal  Paralysis  of  Adults. 

3.  Paralysis  Ascendens  Acuta. 

4.  Chronic  Atrophic  Spinal  Paralysis. 

III.  Spinal  Atrophic  Paralyses.  -{  5.  Peri-ependymal  Myelitis— Syringomyelia. 

6.  Progressive  Muscular  Atrophy. 

7.  Primary  Labio-glosso-laryiigeal  Paralysis. 

8.  Ophthalmoplegia  Externa. 
t  9.  (Pseudo-hypertrophic  Paralysis.) 

II.  Cerebro-spinal  or  Spasmodic  Paralyses. 

1.  Primary  Lateral  Sclerosis. 

2.  Compound  Lateral  Sclerosis. 
a.  Amyotrophic  Lateral  Sclerosis. 
6.  Combined  Posterior  &  Lateral  Sclerosis. 

3.  Secondary  Lateral  Sclerosis. 

a.  Compression  Myelitis. 

b.  Transverse  Myelitis. 

1.  Tonic  Spasm.     I    "  j     ^  >r>       J- 
(.  b.  Late  Rigidity. 

f  a.  Intermittent  Tremor. 
I  b.  Choreiform  Movements. 

2.  Tonic  &  Clonic  '  i.   Pre-hemiplegic  Chorea, 
ii.  Post-hem iplegic  Chorea. 

iii.  Spastic  Hemiplegia  of 

Infancv. 


I.  Spinal  Spasmodic  Paralyses. 
(paraplegia.) 


II.  Cerebral  Paralyses. 
(hemiplegia.) 


Spasm. 


3.  Clonic  Spasm. 


I 

f  a.  Continuous  or  Remittent 

!  Tremors. 

J 

j  b.  Athetosis. 

[  c.  Post-heniiplegic  Hemiataxia. 


III.  Mixed  Paralysis. 

B.  FUNCTIONAL  PARALYSES. 

(1)  Toxic  Paralysis. 

(2)  Febrile  and  Post-febrile  Paralysis. 

(3)  Reflex  Paralysis. 

(4)  Post-epileptic  Paralysis. 
(.5)  Hysterical  Paralysis. 


172 


CxENEKAL    SYMPTOMATOLOGY. 


Table  II.— Paralyses  from  Organic  Disease  of  the  Nervous  System. 

TOPOGRAPHICAL  DIAGNOSIS. 

I.  Spino-neural  Lesions. 

I.  LESIONS  OF  EFFERENT  NERVE  FIBRES. 

II.  LESIONS  OF  AFFERENT  NERVE  FIBRES. 
III.    LESIONS  OF  THE  ANTERIOR  GRAY 


CLINICAL  DIAGNOSIS. 
I.  Atrophic  Paralyses. 

I.  NEURAL  or  peripheral    PARALYSES. 

II.  REFLEX  ATROPHIC  PARALYSIS. 

III.  SPINAL  ATROPHIC  PARALYSES. 


1.  Acute  Atrophic  Spinal  Parah'sis 

of  Infants. 

2.  Acute  Atrophic  Spinal  Paralysis 

of  Adults. 

3.  Acute  Ascending  Paralysis. 

4.  Chronic  Atrophic  Spinal  Paralysis. 
.5.  Peri-ependymal  Myelitis.  "] 

6.  Progressive  Muscular  Atrophy.  i 

7.  Primary  Labio-glosso-laryngeal 

Paralysis. 

8.  Ophthalmoplegia  Externa. 

9.  (Pseiido-hypertrophic  Paralysis.) 

II.  Spasmodic  Paralyses. 

I.  spinal  spasmodic  paralyses. 

1.  Primary  Spinal  Spasmodic  Paralysis. 

2.  Compound  Spinal  Spasmodic 

Paralysis. 

3.  Secondary  Spinal  Spasmodic 

Paralysis. 

II.    CEREBRAL  PARALYSES. 


1.  Ordinary  Hemiplegia. 

2.  Alternate  Hemiplegia. 

3.  Hemiplegia  and  Hemianc^sthesia. 

4.  Hemiplegia,  Hemianaasthesia,  and 

Hemianopsia 

5.  Pre-hemiplegic  Chorea. 

6.  Post-hemiplegic  Chorea. 

7.  Athetosis. 

8.  Post-hemiplegic  Continuous 

Tremor  and  Hemiataxia.  j 

9.  Spastic  Hemiplegia  of  Infancy. 

10.  Unilateral  Convulsions  and 

Hemiplet 


HORNS.     (POLIOMYELOPATHIES.) 

Poliomyelitis  Anterior  Acuta 

Infantium. 
Poliomyelitis  Anterior  Acuta 

Adullorum. 
Poliomyelitis  Acuta. 
Poliomyelitis  Anterior  Chronica. 

Degeneration  of  the  Ganglion  Cells  of 
the  Anterior  Horns  of  the  Spinal 
Cord  and  Motor  Cells  of  the  Me- 
dulla Oblongata. 

(Primary  Muscular  Disease.) 

II.  Cerebro-spinal  Lesions. 

(PYRAMIDAL  TRACT.) 
.    LESIONS  OF  THE  LATERAL  COLUMNS. 

Primary  Lateral  Sclerosis. 

Amyotrophic  Lateral  Sclerosis. 

Combined  Posterior  and  Lateral 

Sclerosis. 
/  Compression  Myelitis. 
l  Transverse  Myelitis. 

II.  LESIONS  OF  THE  CEREBRAL  PYRA- 
MIDAL TRACT  AND  MOTOR  AREA  OF 
CORTEX. 

r  Lesions  of  Lenticular  Nucleus. 
I  Area  of  Lenticulo-striate  Artery. 

Lesions  of  Crura  and  Pons. 

Lesions  in  Area  of  Opto-striate  Artery. 


Lesions  in  the  Area  of  the  Posterior 
External  Optic  Artery. 


f  Unilateral  Atrophy  of  the  Motor 
Area  of  Cortex. 
Porencephalus. 
Lesions  of  Motor  Area  of  Cortex. 


THE    EXTERNAL    KINESIONEU  ROSES.  173 

3.  Reflex  Central  Kinesioneuroses. 

The  disorders  which  occur  in  the  reflex  mechanisms  which  are  situ- 
ated in  the  different  parts  of  the  nervous  system  are  almost  infinitely 
numerous,  but  we  shall  here  mention  only  a  few  of  the  more  usual  dis- 
orders of  the  spinal  reflexes.  The  spinal  reflexes  may  be  divided 
into  (1)  the  superficial,  and  (2)  the  deep  reflexes,  while  disorders  of  the 
reflex  mechanisms  may  declare  themselves  by  way  of  an  excessive  reac- 
tion, constituting  (</)  reflex  hyperkinesis^  or  by  diminution  or  loss  of 
reaction,  constituting  (h)  reflex  akinesis. 

(1)  The  Superficial  Reflexes. 
The  superficial  reflexes  are  excited  by  stimulation  of  the  skin  and 
accessible  mucous  membranes.     The  tests  employed  for  estimating  the 
various  degrees  of  these  reflexes   are  tickling,   pricking,  pinching,  or 
gently  scratching  the  surface,  or  the  application  of  the  faradic  current 
to  the  surface  by  means  of  dry  electrodes  or  the  faradic  brush. 
The  following  superficial  reflexes  may  be  distinguished  (Fig.  70) : 
(ji)  The  plantar  reflex,  obtained  by  tickling  the  sole  of  the  foot  and 
depending  upon  the  integrity  of  the  reflex  loops  through  the  lower  end 
of  the  cord  (conus  meduUaris). 

[b)  The  gluteal  reflex,  consisting  of  contraction  of  the  gluteal  mus- 
cles caused  by  stimulating  the  skin  over  the  buttock,  and  depending 
upon  the  integrity  of  the  loops  through  the  fourth  and  fifth  lumbar 
nerves. 

(c)  The  cremasteric  reflex,  by  which  the  testicle  is  drawn  up  when 
the  skin  on  the  inner  side  of  the  thigh  is  stimulated,  and  demanding 
the  integrity  of  the  first  and  second  pairs  of  lumbar  nerves. 

{d)  The  abdominal  reflex,  consisting  of  a  contraction  of  the  abdominal 
muscles,  chiefly  the  rectus,  caused  by  stroking  the  skin  on  the  side  of 
abdomen  from  the  edge  of  the  ribs  downwards,  and  requiring  the  integ- 
rity of  the  arc  throusrh  the  nerves  from  the  eighth  to  the  twelfth  dorsal 
nerves, 

(g)  The  epigastric  reflex,  producing  a  dimpling  of  the  epigastrium 
on  the  side  stimulated.  It  is  induced  by  stimulation  of  the  side  of  the 
chest  in  the  sixth,  fifth,  and  sometimes  fourth  intercostal  spaces.  This 
dimpling  probably  depends  upon  contraction  of  the  highest  fibres  of 
the  rectus  abdominis,  and  its  presence  requires  the  integrity  of  the  cord 
from  the  fourth  to  the  sixth  or  seventh  pairs  of  dorsal  nerves. 

(/)  The  erector  spinal  reflex,  consisting  of  a  local  contraction  of 
these  muscles,  caused  by  stimulation  of  the  skin  along  their  edge  from 


174 


GENERAL    SYMPTOMATOLOGY. 


< 


Fig  70. 


a 


)0.. 


^.■. 


Motor. 
Sterno-mastoid  .... 

Trapezius ...  .     . 

Khomboids  and  rotators  of 

humerus    .     .  .     . 

Diaphragm    ... 
Deltoid,  biceps,  brachalis, 

supinators. 
Serratus. 
Triceps,      extensors      of 

wrist  and  fingers,  and 

pronators 

Flexors  of  wrist  and  long 

flexors  of  fingers     .     . 

Intrinsic  muscles  of  hand 


•  Sensory. 

Neck  and  scalp. 


Neck  and  shoulder. 


Reflex, 


Intercostal  muscles 


Outer  aspect  of  arm  and 
forearm. 


Anterior  and  posterior  as- 
pects of  arm,  forearm, 
outer  half  of  hand,  and 
•iy,2.  fingers. 

Inner  aspect  of  arm,  fore- 
arm, innerhalf  of  hand, 
and  iYi  fingers. 


Front  of  thorax 
Ensiform  cartilage  , 


"  Scapular. 


Epigastric. 


(-   Abdominal  muscles 


Abdomen  .... 

Umbilicus      .     .     . 

J-  Buttock,  upper  part 


Abdominal 


)! 


Flexors,  hip 


Extensors,  knee 

Adductors        1 

Abductors  ■    Hip 

I 
Extensors  (?)  J 

Flexors,  knee(?) 

Muscles  of    leg    moving 
foot. 


J    Groin  and  scrotum  (front) 

{Outer  side 
Front  side 
Inner  side 


.   J    Thio-h  I  Front  side 


Cremasteric 
Knee-jerk. 


Leg,  inner  side  .     .     .     .  i 

Buttock,  lower  part     .     .  r  Gluteal. 
"  Back  of  thigh    .... 

Leg    and    foot,    except  "I    Foot-chmns. 

inner  part    ....  J    Plantar. 


Perineal  and  anal  muscles        Perineum  and  anus. 
Skin  from  coccyx  to  anus 


DI.1GKA.M    AM,   TaIILE   SHOWING  THE   APPROXIMATE  RELATION   TO   THE   SPINAL   NERVES   OF  THE   VARIOUS   SENSORY   AND 

Reflex  Functions  of  the  Spinal  Cord.    (After  Gowers.) 


THE    EXTERNAL    KINESIONEUROSES.  175 

the  angle  of  the  scapula  to  the  iliac  crest,  and  demanding  the  integrity 
of  the  reflex  arcs  in  the  dorsal  region  of  the  spinal  cord. 

[y)  The  scapular  reflex,  consisting  of  a  contraction  of  some,  or 
nearly  all,  of  the  scapular  muscles  according  to  its  degree,  and  demand- 
ing the  integrity  of  the  cord  at  the  level  of  the  upper  two  or  three 
dorsal  and  lower  two  or  three  cervical  nerves. 

(A)  Ti\Q  palmar  reflex  consists  of  a  contraction  of  the  flexors  of  the 
fingers  induced  by  tickling  the  palm  of  the  hand.  It  requires  the 
integrity  of  the  reflex  arcs  through  the  greater  part  of  the  cervical 
enlargement.  This  reflex  is  not  readily  induced  during  waking  hours 
and  consequent  cerebral  activity,  probably  because  the  hand  is  much 
more  under  cerebral  influence  than  the  foot.  During  sleep,  however, 
and  in  young  infants,  when  the  cerebral  influence  is  suspended,  or  not 
yet  fully  established,  this  reflex  is  as  readily  induced  as  the  reflex  of 
the  sole  of  the  foot. 

{{)  Cranial  Reflexes. — The  chief  reflexes  of  the  cranial  nerves  are 
the  contraction  of  the  palatal  muscles  caused  by  irritation  of  the  fauces  ; 
the  facial  contortions  caused  by  irritation  of  the  fifth  nerve ;  the 
sneezing  and  lachrymation  caused  by  irritation  of  the  mucous  mem- 
brane of  the  nose ;  the  cough  caused  by  irritation  of  the  mucous  mem- 
brane of  the  larynx ;  the  closure  of  the  eyelids  caused  by  irritation  of 
the  conjunctiva  ;  and  the  reflex  contraction  of  the  iris  caused  by  light. 

Some  of  these  reflexes  are  absent  in  healthy  individuals  more  especi- 
ally the  reflexes  of  the  back  and  abdomen,  so  that  the  diminution  or 
absence  of  these  must  not  be  taken  as  a  sure  sign  of  disease.  Their 
presence,  however,  is  a  proof  that  the  respective  paths  through  the 
cord  are  not  seriously  interrupted. 

a.    HTPERKINESIS    OF    THE    SUPEKFICIAL    REFLEXES. 

Increase  of  the  reactions  obtained  from  reflex  stimulation  indicates 
that  the  irritability  of  the  reflex  arc  is  increased  in  some  portion  of  its 
course,  or  that  the  inhibitory  influence  of  the  cerebrum  is  withdrawn. 
Exaggerated  reflex  reactions  are  obtained  by  increased  irritability  (j) 
of  the  afferent  portion  of  the  arc ;  (jj)  of  the  efferent  portion  of  the 
arc ;  ( jjj )  of  the  gray  matter  of  the  cord,  as  in  tetanus  and  strychnia 
poisoning  ;  (iv)  by  arrest  of  the  functions  of  the  pyramidal  tracts  (Fig. 
71,  6,  7).  The  condition  of  the  cutaneous  reflexes  in  cerebral  paral- 
ysis, however,  appears  to  be  an  exception  to  the  rule  that  withdrawal 
of  the  cerebral  influences  causes  excess  of  the  reflex  actions,  inasmuch 
as  the  cutaneous  reflexes  are  diminished  or  lost  on  the  paralyzed  side 
in  hemiplegia.     The  diminution  of  the  cutaneous  reflexes  under  such 


17(3  GENEKAL    SYMPTOMATOLOGY. 

circumstances  is  caused  probably  by  a  loss  of  tone  of  the  muscular 
fibi-es  distributed  to  the  skin,  which  prevents  the  papillae  from  being 
ijroperly  exposed  to  the  irritation  of  tickling  and  other  cutaneous 
stimulants. 

b.    AKINESIS  OF  THK  SUPERFICIAL  REFLEXES. 

When  stinnilation  of  the  surface  produces  either  feeble  or  no  reac- 
tions, it  indicates  that  there  is  diminution  or  loss  of  the  irritability  (j) 
of  the  afferent  portion  of  the  arc — examples  of  which  are  met  with 
in  destructive  lesions  of  the  sensory  branches  of  the  fifth  nerve ;  (jj) 
of  the  efferent  fibres — examples  being  afforded  by  lesions  of  the  facial 
nerve  and  the  anterior  roots  of  the  spinal  nerves  ;  (jjj)  of  tlie  gray 
matter  of  the  anterior  horns — examples  of  which  are  afforded  by  the 
spinal  atrophic  paralyses,  and  by  the  diminution  of  the  reflexes  which 
is  observed  after  large  doses  of  l^romide  of  potassium  ;  and  (iv)  by 
increased  cerebral  action  conveyed  through  the  pyramidal  tracts — an 
example  being  afforded  by  the  inhiliition  of  reflex  actions  by  means  of 

voluntary  control. 

(2)  The  Deep  Keflexes. 

a.  tendon  reactions. 

If  a  man  in  health  sits  with  one  leg  crossed  upon  the  other,  and  the 
ligamentum  ])atellae  be  then  smartly  struck  immediately  below  the  knee- 
cap, the  extensor  muscles  in  front  of  the  thigli  Ijecome  suddenly  con- 
tracted, and  the  foot  is  jerked  forwards  to  a  variable  extent  according 
to  the  degree  of  contraction.  The  jerk  is  named  the  patellar-tendon 
reaction,  knee-phenomenon,  or  knee-jerk.  The  blow  is  usually  deliv- 
ered by  the  inner  edge  of  the  hand ;  but  an  ordinary  stethoscope, 
held  loosely  by  the  small  end  Avhile  the  blow  is  struck  by  the  edge  of 
the  ear-piece,  is  a  convenient  instrument  for  the  purpose,  and  a  Win-  • 
terich  percussion  hammer  is  a  still  more  efficient  instrument.  It  is 
also  desirable  to  uncover  the  knee  that  the  blow  may  be  delivered  on 
the  bare  skin.  In  stout  people,  Avho  cannot  cross  one  leg  over  the 
other  in  a  sitting  posture,  the  operator  may  pass  his  hand  beneath  the 
patient's  thigh  just  above  the  knee-joint,  and,  grasping  the  opposite 
knee,  support  the  extremity  to  be  examined  by  his  forearm.  Another 
convenient  ])osition  is  to  get  the  patient  to  sit  on  a  table  or  on  an 
elevated  seat  with  the  legs  hanging  freely.  Similar  reactions  may  be 
obtained  by  striking  the  tendons  of  the  upper  extremity,  but  these  are 
not  well  marked  except  under  certain  diseased  conditions.  The  reac- 
tions are  best  elicited  by  striking  Avith  the  edge  of  the  stethoscope  the 
tendon  of  the  triceps  at  the  elbow,  and  those  of  the  supinator  longus 
and  extensor  muscles  at  the  wrist. 


THE    EXTEENAL    K INESI OXEU  ROSES .  177 

b.    VARIOUS    FORMS    OF   CLONUS. 

Ankle-clonus^  or  Achilles-tendon  reaction,  consists  of  a  rhytlimical 
clonic  spasm,  which  can  be  obtained  under  certain  circumstances  at  the 
ankle-joint.  When  the  necessary  conditions  are  present,  the  reaction 
is  most  readily  elicited  if  the  operator  will  support  the  lower  extremity 
of  the  patient  by  placing  his  hand  behind  the  knee-joint,  the  leg  being 
slightly  bent  upon  the  thigh,  while  with  the  right  hand  he  seizes  hold 
of  the  toes  lightly  between  the  fingers  and  thumb  and  puts  the  tendo 
Achillis  suddenly  upon  the  stretch  by  producing  a  quick  and  enero-etic 
dorsal  flexion  of  the  foot,  and  then  maintaining  pressure  against  the 
toes  for  some  time.  When  the  tendon  is  first  stretched,  the  sastro- 
cnemius  immediately  contracts  and  the  toes  are  depressed;  the  muscle 
now  relaxes,  and,  the  pressure  of  the  hand  being  still  continued,  the 
toes  are  once  more  elevated,  when  the  muscle  again  contracts  and  de- 
presses the  toes  a  second  time ;  and  thus  the  contractions  and  relaxa- 
tions are  continued  in  rhythmic  sequence  so  long  as  the  tension  of  the 
tendo  Achillis  is  maintained.  This  series  of  rhythmic  contractions 
constitutes  ankle-clonus,  and,  so  long  as  the  movement  continues, 
between  eight  and  ten  contractions  of  the  gastrocnemius  take  place  in 
a  second  of  time. 

Toe-clonus. — In  cases  of  increased  tension  of  the  foot,  rhythmical 
contractions  of  the  big  toe  may  be  obtained  by  producing  sudden  pas- 
sive extension  of  the  first  phalanx,  flexion  being  produced  by  contrac- 
tion of  the  abductor  and  flexor  brevis  pollicis. 

Wrist-elonui^. — Movements  like  those  of  ankle-clonus  may  be  ob- 
tained in  the  hand,  in  cases  of  late  rigidity  of  hemiplegia,  by  grasp- 
ing the  tips  of  the  fingers  and  pressing  the  hand  backwards  so  as  to 
produce  hyperextension  at  the  wrist. 

C.    PERIOSTEAL    AND    FASCIAL    REACTIONS. 

The  best  known  of  these  movements  are  the  contraction  of  the  quad- 
riceps femoris  muscle,  induced  by  gently  tapping  the  front  of  the  tibia 
near  its  middle ;  that  of  the  biceps  on  tapping  the  lower  end  of  the 
radius  with  the  edge  of  the  stethoscope ;  and  that  of  the  triceps  on 
tapping  the  lower  end  of  the  ulna,  in  cases  of  muscular  rigidity  with 
contraction.  When  the  muscles  of  the  shoulder  and  arm  are  impli- 
cated in  the  rigidity,  contractions  of  the  pectoralis  major,  deltoid,  and 
biceps  may  be  obtained  by  a  gentle  tap  on  the  sternal  end  of  the  clavi- 
cle, and  even  a  crossed  reaction  may  be  obtained  by  a  tap  on  the  cla\i- 
cle  of  the  opposite  side.     Under  similar  circumstances  a  considerable 

12 


j^Yg  GENERAL    SYMPTOMATOLOGY. 

number  of  the  muscles  of  the  scapula  and  shoulder  contract  on  tap- 
ping the  spine  of  the  scapula.  Contractions  of  the  erector  muscles  of 
the  spine  may,  under  certain  circumstances,  be  induced  by  tapping  the 
lumbar  fascia. 


d.    SPINAL    EPILEPSY. 


The  paroxysms  of  violent  tremors  which  occur  in  certain  affections 
of  the  spinaf  cord,  and  which  Brown-Sequard  named  spinal  epilepsy 
from  a  fancied  similarity  to  an  epileptic  convulsion,  are  of  a  compound 
nature.  These  movements  appear,  indeed,  to  be  caused  by  contrac- 
tions produced  by  simultaneous  and  successive  stimulations  of  the 
superficial  and  deep  reflexes.  A  painful  cutaneous  impression  causes 
reflex  contractions  of  both  lower  extremities,  which  predominate  in  the 
flexors ;  but  when  the  anterior  flexors  of  the  legs  contract  the  Achilles 
tendons  are  put  upon  the  stretch,  and  ankle-clonus  results.  These 
actions  and  reactions,  reverberating  for  a  time  through  all  the  muscles, 
maintain  the  lower  extremities  in  a  state  of  tremor,  which  may  be  so 
violent  as  to  shake  the  bed  on  which  the  patient  reposes.  When  these 
tremulous  movements  are  proceeding,  if  the  toes  of  one  foot  be  grasped 
by  the  hand  and  brought  suddenly  and  powerfully  into  plantar  flexion, 
the  muscles  iu^mediately  relax  and  the  tremors  cease  for  a  time. 


e.    PARADOXICAL    CONTRACTION. 


Some  muscles  may,  under  certain  circumstances,  be  made  to  contract 
by  suddenly  approximating  their  points  of  origin  and  insertion.  I'he 
curious  fact  that  a  sudden  relaxation  of  a  muscle  causes  it  to  contract 
has  led  Westphal,  who  was  the  first  to  direct  attention  to  this  phenome- 
non, to  name  it  paradoxical  contraction.  This  symptom  is  best  studied 
in  the  tibialis  anticus,  which  may,  in  certain  nervous  diseases,  be  made 
to  contract  by  producing  a  sudden,  or  sometimes  a  gradual,  dorsal 
flexion  of  the  foot.  When  the  patient  is  laid  on  his  back  in  l)ed,  and 
the  muscles  are  relaxed,  the  feet  occupy  the  position  of  extensor  or 
plantar  flexion.  If  dorsal  flexion  of  the  foot  be  now  produced,  the 
tibialis  anticus,  under  certain  not  well-ascertained  circumstances,  enters 
into  contraction,  its  tendon  becomes  prominent,  and  the  foot  is  main- 
tained for  some  minutes  in  the  position  of  dorsal  flexion  and  adduction. 
Distinct  resistance  is  also  offered  to  the  production  of  plantar  flexion  of 
the  foot  by  passive  movements.  After  a  variable  interval  of  time  the 
muscle  relaxes,  either  gradually  and  continuously  or  with  several  inter- 
missions, and  the  foot  falls  by  its  own  weight  to  the  position  of  plantar 
flexion.    The  paradoxical  contraction  sometimes  extends  to  the  extensor 


THE    EXTERNAL    KINESIONEUROSES.  179 

communis  digitorum  and  extensor  brevis  pollicis.  It  is  possible  that 
this  anomalous  reaction  is  caused  by  an  impression  upon  the  sensory 
nerves  of  the  joints,  and  not  by  the  sudden  relaxation  of  the  muscle. 

/.    HTPERKIXESES    OF    THE    DEEP    REFLEXES. 

(j)  It  is  probable  that  increased  irritability  of  both  the  aflFerent  and 
efferent  portions  of  the  reflex  arcs  will  increase  the  activity  of  these 
reactions,  but  no  crucial  examples  of  this  kind  have  as  yet  been  de- 
scribed. When,  however,  the  irritability  of  the  muscular  fibres  them- 
selves is  increased  in  degree,  as  in  phthisis  and  other  exhausting  diseases, 
the  tendon  reactions  are  much  more  readily  induced  than  in  health. 

(jj)  Irritation  of  the  posterior  roots,  and  of  the  efferent  fibres  as 
they  pass  through  the  inner  radicular  fiisciculus  of  the  posterior  col- 
umns, probably  also  increases  the  activity  of  the  tendon  reactions,  but 
direct  evidence  upon  this  point  is  as  yet  wanting. 

(jjj)  Increased  irritability  of  the  gray  substance  of  the  spinal  cord 
causes  increase  of  the  activity  of  the  tendon  reactions.  The  patellar- 
tendon  reaction  is,  for  example,  exaggerated  by  the  administration  of 
strychnia,  and  probably  also  by  such  diseases  as  tetanus  and  hydro- 
phobia. 

(iv)  The  tendon  reactions  are  increased  in  activity  when  the  cerebral 
influence  is  withdrawn  from  the  spinal  cord  by  disease  of  the  pyramidal 
tracts,  and  consequently  all  these  reactions  are  exaggerated  in  all  forms 
of  sj)asmodic  paralysis,  unless,  indeed,  the  reflex  arc  is  at  the  same 
time  arrested  by  a  local  spinal  disease  like  chronic  spinal  pachymenin- 
gitis. 

g.    AKINESES  OF  THE  DEEP  REFLEXES. 

(j)  The  tendon  reactions  are  diminished  or  lost  in  disease  of  the 
afferent  portion  of  the  reflex  arc.  The  disease  may  be  situated  in  the 
tendon  itself;  in  such  a  case  the  movements  of  the  joint  are  generally 
interfered  with  by  an  ankylosis,  and  the  conditions  are  not  favorable 
for  applying  the  test.  The  reaction  may  be  lost  when  the  lesion  is 
situated  in  the  peripheral  course  of  the  nerve  (Fig.  71,  1),  but  the 
motor  and  sensory  fibres  are  then  interfered  with,  and  under  such 
circumstances  it  is  not  possible  to  prove  that  disease  of  the  afferent 
fibres  takes  any  part  in  the  arrest  of  the  reaction.  This  reaction  may, 
however,  be  lost  in  spinal  meningitis  affecting  the  posterior  roots 
(Fig.  71,  2),  when  the  absence  of  any  atrophic  paralysis  of  the  cor- 
responding muscle  shows  that  the  afferent  portion  of  the  reflex  arc  is 
intact.     The  patellar-tendon  reaction  is,  for  instance,  often  absent  in 


180 


GENERAL    SYMPTOMATOLOGY 


(ii)  This  reaction  is  lost  when  the  afferent  fibres  are  diseased  in 
their  passage  through  the  inner  radicular  fasciculus  (Fig.  71  3)  of  the 
pachymeningitis  affecting  the  lumbar  region  in  the  absence  of  any  atro- 
phic paralysis  of  the  quadriceps  femoris  muscle. 


Fig.  71. 


Diagram  of  the  Keflex  Functions  of  the  Spinal  Coed.  (Young. 
C,  skin  and,  T,  tentlon  with  their  afl'erent  nerve  fibres,  both  terminating  in  the  ganglion  cell  of  the  anterior 
gray  horn,  from  which  issues  an  efferent  fibre  which  connects  the  cell  with  the  muscle  M.  B  B,  the  cor- 
tices of  the  cerebral  hemispheres,  with  their  attached  pyramidal  tract  fibres  connecting  the  cortical  giant 
cells  with  the  ganglion  cells  of  the  anterior  gray  horns.  1,  lesion  of  the  peripheral  nerve,  causing  atrophic 
paralysis,  loss  of  sensation,  and  abolition  of  both  kinds  of  reflexes  ;  2,  lesion  of  the  posterior  root  (pachy- 
meningitis), causing  loss  of  sensation  and  abolition  of  both  kinds  of  reflexes,  but  no  paralysis  ;  3,  lesion 
of  the  posterior  root-zone  (tabes  dorsalis),  causing  loss  of  the  tendon  reflex  only  ;  4.  lesion  of  the  anterior 
gray  horns  (poliomyelitis),  causing  atrophic  paralysis  and  loss  of  both  kinds  of  reflexes,  but  no  sensory 
disorder  ;  5,  lesion  of  the  anterior  root  (pachymeningitis),  causing  the  same  symptoms  as  4 ;  C,  transverse 
lesion  of  the  spinal  cord,  causing  a  spasmodic  paralysis  of  the  lower  extremities,  with  excess  of  both 
kinds  of  reflexes  ;  7,  focal  lesion  of  the  cerebral  hemisphere,  causing  hemiplegia  of  the  opposite  side,  with 
excess  of  the  tendon  reflexes  on  the  paralyzed  side,  but  with  diminution  of  the  cutaneous  reflexes.  The 
dotted  lines  indicate  descending  sclerosis  of  the  pyramidal  tracts 

spinal  cord,  this  being  the  essential  anatomical  change  in  locomotor 
ataxia.  It  will  hereafter  be  found  that  loss  of  the  patellar-tendon 
reaction  is  the  earliest  and  most  constant  symptom  of  locomotor  ataxia. 


THE    EXTERXAL    KI XESIONEU  ROSES .  181 

(jjj)  Tlie  tendon  reactions  are  diminished  or  lost  in  depressive  and 
destructive  lesions  of  the  gray  anterior  horns.  Large  doses  of  bromide 
of  potassiinn  and  of  opium  diminish  the  activity  of  the  tendon  reaction 
and  it  is  very  probable  that  a  poison  circulates  in  the  blood  which 
diminishes  or  abolishes  these  reactions  in  certain  cases  of  diabetes. 
Destructive  lesions  (Fig.  71,  4)  of  the  anterior  gray  horns  abolish 
the  tendon  reactions,  but  the  loss  of  the  reactions  is  accompanied  by 
paralysis  with  atrophy  of  the  corresponding  muscles. 

(iv)  The  tendon  reactions  are  likewise  lost  in  destructive  lesions  of 
the  efferent  portion  of  the  reflex  arc  (Fig.  71,  5),  and  in  this  case,  also, 
the  abolition  of  the  reaction  is  accompanied  by  paralysis  with  atrophy 
of  the  muscles.  Disease  of  the  muscle  itself  abolishes  the  reflex,  the 
early  loss  of  the  patellar-tendon  reaction  in  pseudo-hypertrophic  paral- 
ysis being  a  good  example. 

(v)  Increase  of  cerebral  influence  on  the  gray  substance  of  the  spinal 
cord  diminishes  the  activity  of  the  tendon  reactions.  The  patellar- 
tendon  reaction  can,  for  instance,  be  arrested  by  voluntary  eifort,  and 
it  is  diminished  or  lost  during  the  convulsive  stage  of  an  epileptic 
attack.  The  conditions  under  which  paradoxical  contraction  is  ob- 
tained are  not  well  ascertained. 

h.    AUTOMATIC    KINESIONETJROSES. 

The  groups  of  symptoms  which  may  be  included  under  automatic 
aff'ections  of  the  muscles  of  external  relation,  cannot  be  distinctly 
separated  from  the  reflex  and  voluntary  afi'ections  of  these  muscles. 
There  are,  however,  disturbances  of  muscular  adjustments  in  which  the 
simple  reflex  actions  of  the  spinal  cord,  the  sensory  mechanisms,  and 
the  voluntary  mechanisms  are  normal,  and  yet  in  which  complex  mus- 
cular adjustments  either  fliil  to  be  efiected  in  spite  of  all  voluntary 
efforts  to  accomplish  them,  or  are  effected  in  spite  of  all  voluntary 
efforts  to  prevent  them,  the  last  kind  of  adjustment  being  named  com- 
pulsory ov  forced  movements.  It  is  such  movements  as  these  Avhich 
are  meant  to  be  included  under  the  name  of  automatic  kinesioneuroses 
of  the  muscles  of  external  relation.  These  movements  are,  in  all  proba- 
bility, coordinated  in  the  cerebellum  and  basal  ganglia  of  the  cerebrum. 

(1)  Peripheral  Auicnnatlc  Disorders. 

Disorder  of  LahjrinfMne  Impressions. — Disease  of  the  peripheral 
nerves  generally  involves  either  the  sensory  or  the  voluntary  motor 
fibres,  or  both  together,  so  that  disorder  of  muscular  coordination 
becomes  thus   obscured  by   the  more  prominent  symptoms  caused  by 


Ig2  GENERAL    SYMPTOMATOLOGY. 

disorder  of  the  voluntary  mechanism.  There  is,  however,  a  growing 
conviction  that  ataxia  is  frequently,  if  not  always,  caused  by  a  periph- 
eral lesion,  but  we  shall  at  present  adhere  to  the  more  classical  view 
that  it  is  caused  by  a  spinal  lesion.  It  would  seem,  however,  that  the 
seventh  pair  of  nerves  contain  afferent  fibres  which  are  not  subservient 
to  the  conduction  of  sensory  impressions,  and  yet  disease  of  which 
gives  rise  to  the  phenomena  of  motor  incoordination.  These  fibres  are 
involved  in  disease  of  the  internal  ear  or  of  the  semicircular  canals,  and 
in  such  cases  the  patient  suffers  from  a  staggering  and  uncertain  gait, 
which  will  be  subsequently  described  as  Meniere's  disease.  The  dis- 
orderly and  incoordinate  movements  of  animals  after  division  of  one  or 
other  of  the  semicircular  canals  are  described  in  manuals  of  physiology. 

(2)  Spinal  Automatic  Disorders. 

Ataxia  is  a  very  characteristic  kind  of  motor  incoordination  observed 
in  diseases  of  the  spinal  cord,  and  constitutes  the  most  prominent 
feature  of  tales  dorsalis.  It  is  characterized  by  inal>ility  to  make 
combined  or  complicated  movements  with  certainty  and  precision,  and 
in  advanced  cases  all  movements  requiring  intricate  and  delicately 
balanced  muscular  adjustment  become  impossible.  The  motor  incoor- 
dination usually  presents  itself  in  tlie  most  marked  manner  during 
locomotion  and  station,  these  being  respectively  named  dynamic  and 
static  ataxia.  These  forms  of  muscular  incooi'dination  will  be  more 
fully  described  when  locomotor  ataxia  is  under  consideration. 

(3)  Encephalic  Aiiiornatlc  Disorders. 

[a)  Reeling  is  the  well-known  gait  of  a  di'unken  man.  It  is  caused 
by  irregular  swaying  movements  of  the  trunk,  from  side  to  side  and 
from  before  backwards,  requiring  the  legs  to  be  moved  irregularly  in 
various  directions  in  order  to  maintain  their  position  vertically  under 
the  trunk.  Staggering  is  a  slighter  degree  of  motor  incoordination 
than  reeling,  and  vertigo  is  the  subjective  correlation  of  this  form  of 
motor  disorder. 

(5)  OerebeUar  rigidity  consists  of  i-igidity  of  the  muscles  of  the 
neck,  which  in  aggravated  cases  extends  to  those  of  the  back  and 
extremities,  so  that  complete  opisthotonos  is  induced.  This  form  of 
rigidity  is  frequently  associated  with  tumor  of  the  middle  lobe  of  the 
cerebellum. 

i.    COMPULSORY    OR    FORCED    MOVEMENTS— COORDINATE   CRAMPS. 

These  movements  are  best  seen  in  animals  after  experimental  injury 
to  various  parts  of  the  medulla,  pons,  and  crura  cerebri,  but  most  of 


THE    EXTERNAL    K  IX  ESTON  E  U  ROSES  .  183 

them  are  probably  caused  by  injury  to  one  or  other  of  the  peduncles  of 
the  cerebellum.  The  usual  forms  of  these  movements  are,  that  in  which 
the  animal  rolls  around  the  longitudinal  axis  of  its  OAvn  body,  that  in 
which  it  moves  round  and  round  in  a  circle,  and  that  in  which  it  rotates 
round  the  transverse  axis  of  the  body,  tumbling  head  over  heels  in  a 
series  of  somersaults.  INIovements  of  this  kind  are  never  so  marked 
in  man  as  in  animals,  but  less  degrees  of  these  movements  are  some- 
times observed  in  disease  in  the  neighborhood  of  the  peduncles  of  the 
cerebellum. 

All  the  automatic  disorders  just  described  are  caused  by  the  over- 
throw of  the  delicate  balance  of  the  tonic  muscular  contractions,  which 
is  necessary  for  the  maintenance  of  complicated  adjustments  in  space. 
Irritative  lesions  of  the  cortex  of  the  cerebellum,  which  is  the  organ 
for  regulating  these  tonic  contractions,  gives  rise  to  excessive  tonic  con- 
tractions of  certain  muscles,  which  destructive  lesions  cause  paralysis 
of  them,  Avhich,  however,  is  not  recognized  as  a  paralysis,  because  the 
cerebi-al  influence  on  the  muscles  is  still  intact.  In  other  cases  the 
cerebellum  itself  is  healthy,  but  false  intelligence  is  sent  to  it  owing  to 
disease  of  the  cerebello-afferent  conducting  paths,  and  this  leads  to  a 
loss  of  the  balance  of  the  tonic  contractions  of  the  body,  or  to  loss  of 
equilibration,  as  it  is  called. 

k.    SYNKINESIS. 

Under  this  term  are  generally  included  certain  involuntary  move- 
ments of  paralyzed  parts,  but  we  shall  also  include  under  it  certain 
motor  disorders  which  occur  in  muscles  aifected  with  spasm,  as  w^ell  as 
certain  anomalous  movements  which  occur  in  muscles  that  in  health 
are  associated  in  their  actions  Avith  those  primarily  affected. 

(1)  Associated  Movements  of  Paralyzed  Parts. 

In  facial  paralysis  of  cerebral  origin  the  muscles  of  the  paralyzed 
half  of  the  face  may  occasionally  perform  the  movements  necessary  to 
changes  of  expression  in  association  with  those  of  the  opposite  side, 
although  in  most  cases  the  contrast  between  the  actions  of  the  two  sides 
is  rendered  all  the  more  evident  under  changes  of  expression.  In  cases 
of  hemiplegia  automatic  movements  may  occur  in  a  completely  para- 
lyzed arm.  When  the  patient  sneezes,  and  under  the  influence  of 
emotional  excitement,  the  paralyzed  extremities  may  be  strongly  flexed, 
while  the  unaffected  limbs  remain  passive.  A  voluntary  movement  of 
the  healthy  side  is  often  accompanied  by  a  contraction  of  the  corre- 
sponding muscles  on  the  paralyzed  side. 


184  GEXEEAL    SYMPTOMATOLOGY. 

(2)  Relative  Immuniiy  of  some  Muscles  from  Paralysis,  and  their  Relative  Liability 

to  Convulsion. 

In  ordinary  cases  of  severe  hemiplegia  some  muscles  are  completely 
paralyzed,  while  others  are  little  if  at  all  affected.     The  muscles  which 
are  most  paralyzed  are  those  of  the  extremities  and  the  lower  muscles  of 
the  face,  and  those  which  escape  are  the  muscles  of  the  trunk,  and  the 
upper  muscles  of  the  face.     In   unilateral  convulsions,   however,   the 
spasm  keeps  limited  to  one-half  of  the  body  in  the   extremities  and 
lower  half  of  the  face,  while  it  often  extends  to  both  sides  in  the  trunk 
and  upper  part  of  the  face.     Looking  broadly   at  the  muscles  which 
are  most  liable  to  be  completely  paralyzed  in  hemiplegia,  it  may  be  sai<l 
of  them  that  they  are  the  muscles  which  are  most  engaged  in  executing 
special  movements,  while  those  least  liable  to  be  paralyzed  are  engaged 
in  effecting  the  most  general  movements.     The  muscles  of  the  hand, 
for.  instance,  which  are  so  peculiarly  liable  to  be  paralyzed,  effect  the 
special  movements  of  writing,  while  those  of  the  trunk,  which  generally 
escape,  are  those  which  are  engaged  in   carrying  on  respiration  and 
other  automatic  actions.     But  the  laryngeal   muscles  are  engaged  in 
effecting  the  very  special  movements  of  articulation,  and  yet  they  are 
by  no  means  liable  to  be  affected  in  hemiplegia,  and  consequently  the 
rule  just  laid  down  is  not  of  universal  application,  and  we  may,  there- 
fore, be  certain  that  the  muscles  which  remain  comparatively  free  from 
paralysis  have  some  other  common  characteristic.     This  characteristic 
is  to  be  found  in  the  fact,  first  pointed  out  by  Dr.  Broadbent,  that  tlie 
muscles  wliicli  have  a  relative  immunity  from  paralysis  are  those  which 
are  hilaterally  associated  in  their  actions.     The  thoracic,  abdominal, 
and  laryngeal  muscles,  and  even  those  of  the  eyelids  and  eyebrows  are 
brought  into  simultaneous  action  on  both  sides  of  the  body,  while  those 
of  the  limbs,  and,  to  a  less  extent,  those  of  the  lower  part  of  the  face, 
act  more  or  less  independently  of  one  another  on  the  two  sides.     This 
bilateral  association  of  the  functions  of  certain  groups  of  muscles  Avould 
lead  us  to  expect  that  there  will  be  a  corresponding  bilateral  a-ssociation 
of  the  nervous  mechanisms  by  which  their  movements  are  regulated. 
Dr.  Broadbent  has  suggested  that  in  bilaterally  associated  actions  the 
muscles  of  each  side  are  connected  with   the  cortical   centres  in  both 
hemispheres.     He  believes  that  this  connection  is  effected  by  means  of 
spinal  commissural  fibres,  and    has   happily  enunciated  the  principle 
as  the  bilateral  association  of  the  nerve  nuclei  of  muscles  hilaterally 
associated  in  their  actions.     In  Fig.  72,  for  instance,  d',  representing 
the  spinal  nuclei  of  the  dorsal  nuclei  of  the  left  side,  is  connected  with 
the  cortex  of  the  opposite  side  by  fibres  (5  5)  which   ascend  in  the 


THE    EXTERNAL    KIX  ESI  OX  EU  ROSES  .  185 

pyiamidal  tract,  and  also  with  that  of  the  same  side  througli  the  com- 
raissural  fibres  which  connect  the  two  spinal  nuclei  (<?'"),  and  the  fibres 
(")'  5')  which  connect  the  nuclei  of  the  right  side  (d)  with  the  left 
cortex  {c').  Suppose  now  that  the  fibre  5  5  is  ruptured  and  the  nucleus 
d'  is  thus  severed  from  the  cortex  of  the  opposite  hemisphere,  Avhich 
usually  controls  its  function,  it  can  still  obtain  impulses  from  the  cortex 
of  the  same  side  through  5'  5'  and  c'".  When,  however,  the  muscles 
of  the  opposite  sides  act  independently  of  each  other,  such  as  those  of 
the  right  and  left  hands,  commissural  fibres  are  not  established  between 
their  nerve  nuclei.  In  the  nucleus  (a)  of  the  right  upper  extremity, 
as  represented  in  the  figure,  rupture  of  fibre  6'  severs  the  connection 
with  the  cortex  of  the  opposite  side,  and  no  channel  is  established  l)y 
means  of  which  it  can  obtain  impulses  from  the  cortex  on  the  same  side. 
The  effect  which  this  bilateral  fusion  of  the  spinal  nerve  nuclei  of 
various  nerves  produces  in  certain  spasmodic  affections  is  as  striking  as 
that  produced  by  it  in  hemiplegia.  In  unilateral  chorea,  for  instance, 
while  the  spasmodic  action  is  limited  to  one  side  in  the  extremities  and 
lower  muscles  of  the  ftice,  it  extends  to  the  muscles  of  both  sides  of 
the  trunk  and  of  the  eyelids  and  eyebrows,  these  being  muscles  which 
are  habitually  associated  in  their  actions.  This  rule  is  also  true  with 
respect  to  other  forms  of  convulsion,  so  that  in  hemispasm  the  muscles 
which  are  habitually  associated  in  their  actions  are  affected  on  both 
sides  ;  while  in  hemiplegia  these  muscles  are  comparatively  preserved 
from  paralysis.  The  reason  of  this  is  so  plain  that  it  is  scarcely  neces- 
sary to  add  another  word  by  Avay  of  explanation.  Suppose  that  ex- 
cessive impulses  are  sent  down  from  the  cortex  of  the  brain  through 
the  fibres  6'  and  5',  the  former  will  reach  a  and  pass  out  through  hn 
to  the  muscles  of  the  arm  on  the  opposite  side ;  while  the  latter  will 
i-each  d  and  pass  both  through  dn  and  c'",  d',  and  dn'  to  reach  the 
muscles  of  the  trunk  on  both  sides.  But  the  muscles  which  are  habit- 
ually associated  in  their  actions  are  not  always  symmetrically  placed 
on  the  two  sides  of  the  organism,  nor  are  their  actions  always  analogous. 
It  is  only  necessary  that  their  actions  should  concur  to  produce  a  defi- 
nite result :  and  the  commissural  fibres  often  connect,  not  two  nerve 
nuclei  on  the  same  spinal  level,  but  nuclei  at  different  levels,  thus  form- 
ing an  oblique  crossed  connection  as  in  Fig.  72,  e^. 

(3)   Conjugate  Deviation  of  the  Eyes,  and  Roraiion  of  ihe  Head  and  Neck. 

The  actions  of  the  external  rectus  of  one  eye  and  of  the  internal  of 
the  other  is  a  good  example  of  muscles  having  quite  opposite  actions, 
and  yet  concurring  to  produce  a  harmonious  result.     It  is  evident  that 


186 


G  E  N  E  E  A  L    SYMPTOMATOLOGY. 


if  commissural  connections  exist  anywhere  they  must  exist  between  the 
nucleus  of  the  sixth  nerve  of  one  side  and  the  portion  of  the  nucleus 
of  tiie  third  nerve  which  presides  over  the  action  of  the  internal  rectus 
of  the  opposite  eye ;  and  as  these  nuclei  are  placed  at  different  levels 
in  the  pons  and  crura,  the  connection  between  them  must  be  oblique 
and  crossed.  In  Fig.  72,  let  r  and  r'  represent  respectively  the  nucleus 
of  the  portion  of  the  third  nerves  (3w  and  3w')  supplied  to  the  right 
and  left  internal  recti,  and  er  and  or'  be  respectively  the  nuclei  of  the 

Fig.  72. 


( ',  (",  corte.x  of  ii<;lit  and  left  cereliral  hemi- 
spheres respectively  ;  1,  2,  3,  4,  5,  0,  fihrcs  of  the 
pyramidal  trart  uniting  (',  tlie  cortex  of  the  right 
}iemi8i>Iiere,  and  r',  e'r,  v',  u',  d',  I',  the  respective 
spinal  nuclei  of  the  internal  rectus,  and  the  e.\- 
ternal  rectus  muscles  of  the  eye,  the  muscles  of 
articulation  and  vocalization,  those  of  the  upper 
e.xtremity,  the  dorsal  muscles,  and  those  of  the 
lower  extremity,  all  of  the  left  side  ;  1',  2',  3',  4', 
5',  C,  fibres  of  the  pyramidal  tract,  connecting 
the  corte.x  of  the  left  h('mis]ihere  with  r,  et;  v, 
a,  d,  1,  the  spinal  nuclei  of  the  right  side  cor- 
responding to  those  already  enumerated  on  the 
left  side ;  c,  e,  fihres  of  the  corpus  callosum 
uniting  identical  regions  of  the  two  hemispheres; 
c',  comnn'ssural  fibres  connecting  the  spinal  nu- 
cleus of  the  internal  rectus  muscle  of  one  eye  with 
that  of  the  external  rectus  muscle  of  the  opposite 
eye  ;  c",  those  connecting  the  spinal  nuclei  of  the 
muscles  of  vocalization  and  articulation  of  tho 
two  sides;  c'",  those  connecting  the  special  nuclei 
of  the  muscles  of  the  trunk:  c*,  those  connecting 
the  spinal  nuclei  of  the  posterior  extremity  of 
one  side  witli  the  anterior  extremity  of  the  oppo- 
site side.  The  arrows  indicate  the  direction  of 
the  conduction. 


right  and  left  sixth  nerves  {6n  and  G>i/) :  while  c'  represents  the  cross- 
mg  of  the  commissural  fibres.  The  external  rectus  of  one  eye  and  the 
mternal  of  the  other  eye  acting  simultaneously  rotate  both  eves  so  as 
to  direct  the  axes  of  vision  to  lateral  objects.  When  the  object  is 
placed  to  the  right  it  is  manifest  that  the  right  eye  is  in  a  better  posi- 


THE    EXTKRNAL    KINESIONE  Ul?  OSES  187 

tion  than  the  left  to  catch  the  first  glimpse  of  it,  hence  the  external 
rectus,  Avhich  rotates  the  right  eye  outwards,  takes  the  lead  in  the  action. 
But  the  internal  rectus  of  the  opposite  side  rotates  at  the  same  time  the 
left  eye  inwards :  and  to  effect  this  movement  it  will  be  a  clear  gain  of 
time,  as  well  as  economy  of  force,  if  it  were  to  receive  its  impulses  to 
action  through  the  short  commissural  fibres  which  connect  the  two 
nuclei,  and  not  from  the  cortex  of  the  cerebrum  of  the  opposite  side. 
When,  therefore,  the  eyes  are  directed  by  a  voluntary  effort  to  the 
right,  the  impulse  to  action  may  be  supposed  to  come  from  the  cortex 
of  the  brain  (C)  on  the  opposite  side,  to  pass  out  through  the  fibres 
(2')  of  the  pyramidal  tract  which  connect  the  cortex  with  the  nucleus 
of  the  sixth  nerve  {er'),  and  then  to  pass  on  through  the  commissural 
fibres  (c')  to  the  part  of  the  nucleus  (r)  of  the  opposite  third  nerve 
concerned  in  the  action.  According  to  this  statement,  therefore,  in 
directing  the  eyes  laterally,  say  to  the  right,  both  the  right  external 
rectus  and  the  left  internal  rectus  receive  the  impulse  to  action  from 
the  cortex  of  the  left  hemisphere,  the  impulses  of  the  nucleus  of  the 
third  nerve  being  received  through  the  commissural  fibres  which  con- 
nect it  with  the  nucleus  of  the  sixth  nerve  of  the  opposite  side.  So 
far,  Ave  have  only  spoken  of  the  two  recti  muscles;  but  when  these 
muscles  are  contracting  so  that  the  eyes  are  directed  laterally,  the 
muscles  which  rotate  the  head  also  become  contracted  in  such  a  way 
that  the  head  is  turned  in  the  same  direction  as  the  eyes,  this  movement 
being  frequently  observed  when  a  man  looks  over  his  shoulder.  Rota- 
tion of  the  head,  say  to  the  right,  is  produced  mainly  by  contraction  of 
the  right  inferior  oblique  muscle  of  the  neck,  although  the  left  sterno- 
mastoid,  and  probably  other  muscles,  cooperate  in  the  movement,  and 
these  muscles  also  receive  their  voluntary  impulses  to  action  through 
commissural  fibres  which  connect  their  nerve  nuclei  with  the  nucleus  of 
the  sixth  nerve  of  the  right  side.  According  to  this  supposition,  when 
a  strong  impulse  is  sent  from  the  left  cortex  (C)  of  the  brain  through 
the  fibres  ('2')  which  connect  it  with  the  nucleus  {er)  of  the  sixth  nerve 
of  the  opposite  side,  these  impulses  will  also  pass  through  commissural 
fibres  to  the  nuclei  of  the  nerves  which  supply  the  internal  rectus  and 
sterno-cleido-mastoid  muscles  of  the  opposite  side,  and  of  the  inferior 
oblique  muscle  of  the  neck  of  the  same  side  ;  and  the  eyes  and  head 
will  consequently  be  strongly  rotated  to  the  right,  and  away  from  the 
hemisphere  from  which  the  impulses  originated.  But  this  lateral  devi- 
ation or  conjugate  deviation  of  the  eyes,  as  it  is  called,  occurs  fre([uently 
in  disease,  and  it  is  then  associated  with  rotation  of  the  head  and  neck 
to  the  same  side  as  the  eyes  are  directed.  This  position  of  the  eyes 
and  head  is  almost  a  constant  accompaniment  of  convulsions  of  cereljral 


188  GENERAL    SYMPTOMATOLOGY. 

orio-in,  and,  when  the  convulsions  are  unilateral  and  due  to  disease  of 
the  cortex  of  one  hemisphere,  the  rotation  always  takes  place  towards 
the  convulsed  side  and  away  from  the  seat  of  the  lesion.  Unilateral 
convulsions  are  often  associated  with  a  certain  degree  of  hemiplegia, 
the  convulsions  being  then  limited  to  the  paralyzed  side ;  and  when, 
under  these  circumstances,  conjugate  deviation  of  the  eyes  occurs,  the 
rotation  is  always  towards  the  paralyzed  side.  This,  then,  constitutes 
spasuiodic  lateral  deviation  of  the  head  and  eyes.  But  Graux  has 
drawn  attention  to  the  fact  that  this  lateral  deviation  is  often  of  para- 
lytic origin.  Let  us  now  suppose  that  the  fibres  (2')  which  connect 
the  left  cortex  (C)  and  the  right  nucleus  of  the  sixth  (er)  are  suddenly 
interrupted,  the  cerebral  impulses  to  the  nucleus  are  arrested,  the  ex- 
ternal rectus  of  the  right  eye  becomes  paralyzed,  and  that  eye  is  rotated 
to  the  left.  But  the  impulses  through  the  commissural  fibres  which 
connect  the  nucleus  of  the  right  sixth,  and  those  of  the  left  internal 
rectus,  and  of  the  rotators  of  the  head  to  the  left  must  also  be  arrested, 
so  that  the  latter  muscles  likewise  become  paralyzed ;  hence  the  left 
eye  and  the  head  become,  rotated  to  the  left,  the  rotation  now  taking- 
place  awai/  from  the  paralyzed  side  and  towards  the  hemisphere  of  the 
brain  in  which  the  disease  is  situated.  The  rotation  of  the  eyes  in 
this  direction  has  been  facetiously  described  as  an  attempt  on  the  part 
of  the  patient  to  inspect  the  cerebral  lesion  which  is  the  cause  of  the 
paralysis.  The  rotation  of  the  eyes,  head,  and  neck  is  not  now  due  to 
spasm  of  the  muscles  engaged  in  producing  the  action,  but  to  paralysis 
of  their  antagonists.  This  symptom  is  usually  associated  with  all 
sudden  and  severe  attacks  of  hemiplegia ;  it  is  generally  absent  in  the 
slighter  forms  of  the  attack,  and  in  all  cases  in  which  the  paralysis  is 
more  or  less  gradual  in  its  onset.  The  ])henomenon  is  also,  as  a  rule, 
a  very  transitory  symptom  in  hemiplegia,  and  usually  disappears  in 
from  four  days  to  a  week.  The  rotation  of  the  head  generally  disap- 
pears first,  and  then  the  deviation  of  the  eyes  improves;  but  it  not 
unfrequently  happens  that  a  temporary  s(iuint  may  be  observed  during 
the  progress  of  the  rotation  of  the  eyes  towards  recovery. 

The  reason  of  the  temporary  character  of  the  paralytic  form  of  con- 
jugate deviation  of  the  eyes  and  rotation  of  the  head  and  neck — say 
towards  the  right— appears  to  be  that  although  the  nucleus  of  the  left 
third  {r')  usually  receives  its  impulses  to  action  through  the  commis- 
sural fibres  which  connect  it  with  the  nucleus  of  the  right  sixth  nerve  (er), 
and  consequently  from  the  cortex  of  the  left  hemisphere,  yet  channels 
of  communication  (1)  still  exist  between  the  nucleus  of  the  left  third 
and  the  cortex  of  the  right  liemisphere.  There  is  no  congenital  defi- 
ciency of  the   channels  which   connect  the  cortex  of  the  ri^^ht  hemi- 


THE    EXTERNAL     KIN  ESI  OX  EU  ICOSES  .  189 

sphere  and  the  nucleus  of  the  tliird  nerve  of  the  opposite  side,  nor 
indeed  of  the  oblique  commissural  fibres  -which  connect  the  latter  with 
the  nucleus  of  the  right  sixth  nerve ;  and  now  that  the  more  usual 
channels  are  interrupted  by  disease,  impulses  begin  to  pass  through  the 
k'ss  used  channels.  In  a  few  days,  then,  the  channel  (1)  between  the 
right  cortex  and  the  nucleus  of  the  left  third  nerve  becomes  patent, 
and  some  days  later  the  commissural  fibres  (c)  between  the  two  nuclei 
liecome  so  for  open  as  to  convey  impulses  from  the  nucleus  of  the  left 
third  to  that  of  the  right  sixth,  so  that  the  paralysis  of  the  muscles 
supplied  l)y  these  nerves  disappears.  A  destroying  lesion  in  the  pons 
situated  above  the  nucleus  of  origin  of  the  sixth  nerve,  but  below  the 
upper  crossing  of  the  fibres  of  the  pyramidal  tract,  causes  a  conjugate 
deviation,  Avhich  is  directed  away  from  the  side  of  the  lesion  and 
towards  the  paralyzed  limbs.  It  has  also  been  shown  by  Graux  that 
whereas  disease  of  one  of  the  sixth  nerves  produces  an  internal  squint 
of  the  eye  on  the  side  of  the  lesion,  and  no  affection  of  the  other  eye, 
disease  of  the  nucleus  of  origin  of  one  of  the  sixth  nerves  produces  a 
conjugate  deviation  of  the  eyes,  the  external  rectus  on  the  side  of  the 
lesion  and  the  internal  on  the  opposite  side  being  thus  more  or  less 
'  ])aralyzed.  But  the  internal  rectus  is  not  completely  paralyzed,  although 
it  does  not  act  when  the  eye  has  to  be  directed  to  lateral  objects,  it 
contracts  quite  well  in  association  with  the  internal  rectus  of  the  oppo- 
site eye  when  the  eyes  are  converged  on  a  near  object  in  front.  These 
facts  prove  that  the  internal  rectus  muscle  is  innervated  by  fibres 
issuing  from,  or  at  least  passing  near  the  nucleus  of  origin  of  the  sixth 
nerve  of  the  opposite  side,  as  Avell  as  by  fibres  from  the  third  nerve  of 
the  same  side.  As  we  have  seen,  conjugate  deviation  of  the  eyes  is,  as 
a  rule,  a  transitory  symptom  in  hemiplegia,  but  if  a  lesion  in  the  pons 
•  interrupts  the  commissural  fibres  (c)  so  as  to  prevent  impulses  passing 
from  one  nucleus  to  another,  a  second  lesion  situated  in  any  posi- 
tion which  will  interrupt  the  fibres  of  the  pyramidal  tract  will  then 
produce  a  paralytic  conjugate  deviation  of  the  head  and  eyes  which 
remains  permanent. 

(4)  Secondary  Deviation  of  the  Sound  Eye. 

In  paralysis  of  one  of  the  ocular  muscles,  say  of  the  external  rectus 
of  the  right  side,  the  eye  is  of  course  subject  to  internal  s(piint.  Now, 
if  durino-  recovery  from  this  condition,  when  the  conduction  through 
the  sixth  nerve  (6»)  is  still  delayed,  the  eye  of  the  sound  side  be 
closed  and  the  patient  be  directed  to  look  at  an  object  with  his  right 
eye  in  such  a  way  as  to  strain  the  external  rectus  nuiscle,  this  strain  is 


190  GENERAL    SYMPTOMATOLOGY. 

accompanied  by  a  strong  voluntary  effort,  but  owing  to  the  diminished 
conductivity  of  the  nerve  only  a  relatively  small  amount  of  the  volun- 
tary impulses  will  pass  to  the  muscle.  But  the  impulses  generated  by 
the  strong  voluntary  effort  will  pass  through  the  commissural  fibres  {(■') 
to  the  nucleus  of  the  left  third  nerve  {r')  in  undiminished  degree,  so 
that  the  internal  rectus  of  the  left  eye  becomes  strongly  contracted. 
The  energetic  contraction  of  the  internal  rectus  of  the  left  eye  induces  a 
secondary  squint  in  it,  the  extent  of  Avhich  is  much  in  excess  of  that 
of  the  squint  of  the  paralyzed  side.  But  although  this  secondary 
deviation  is  more  apparent  in  the  case  of  paralysis  of  the  ocular  than 
in  paralysis  of  other  muscles,  yet  essentially  the  same  phenomenon 
occurs  in  the  extremities.  If  the  common  extensor  muscle  of  the  toes 
is  partially  paralyzed,  a  voluntary  effort  to  extend  the  toes  is  followed 
by  flexion  of  them.  A  simple  movement  like  flexion  at  the  elbow-joint 
is  not  caused  by  contraction  of  the  flexors  only,  but  by  the  predominance 
of  their  contractions  over  the  contraction  of  the  extensors  simulta- 
neously induced.  During  recovery  from  an  attack  of  hemiplegia  it 
often  happens  that  when  the  patient  makes  an  effort  to  flex  the  forearm 
the  flexor  muscles  may  be  observed  to  contract,  yet  either  no  movement 
or  movement  in  the  opposite  direction  occurs,  because  the  balance  of 
the  innervation  to  the  antogonistic  muscles  is  equal  to,  or  the  innerva- 
tion to  the  extensors  is  in  excess  of,  that  to  the  flexors. 

(5)  Disorders  of  the  Associated  Movements  of  the  Extremities. 

We  have  seen  that  the  movements  of  the  limbs,  and  especially  of 
the  hand  of  one  side,  are  largely  independent  of  those  of  the  other, 
and  consequently  that  the  spinal  nuclei  of  the  nerves  which  supply  the 
limbs  are  not  intimately  connected  by  transverse  commissural  fibres. 
But  in  walking,  the  movement  of  the  right  leg  is  always  associated 
with  swinging  of  the  left  arm;  and,  conversely,  that  of  the  left  leg  with 
swinging  of  the  right  arm.  It  may  be  inferred,  therefore,  that  the 
nuclei  of  the  nerves  of  the  upper  [a  a')  and  lower  extremities  (/  V)  are 
connected  by  oblique  and  crossed  commissural  fibres.  In  man  the 
movements  of  the  leg  of  one  side  are  not  very  intimately  associated 
with  that  of  the  arm  of  the  opposite  side,  hence  the  commissural  fibres, 
which  connect  their  respective  nerve  nuclei,  are  represented  by  dotted 
lines  (e" ).  In  quadrupeds,  however,  the  crossed  association  between 
the  movements  of  the  anterior  and  posterior  extremities  of  opposite 
sides  IS  much  more  intimate  than  in  man,  and  consequently  the  oblique 
commissural  fibres  are  patent  in  a  corresponding  degree. 

Let  us  now  suppose  that  the  fibres  (4'  and  (J')  which  connect  the 
coitex  (C)  of  the  left  hemisphere  with  the  spinal  nuclei  {a,  I)  of  the 


THE    EXTEENAL    KIN  ESIONEU  ROSES  .  191 

light  extremities  are  ruptured.  Rupture  of  these  fibres  would  produce 
hemipk-gia  in  man ;  but  in  the  dog  only  a  certain  amount  of  paresis 
results,  inasmuch  as  the  right  hind  limb  receives  impulses  through  the 
open  commissural  fibres  which  connect  the  spinal  nuclei  of  its  nerves 
with  the  nuclei  of  the  nerves  of  the  left  anterior  limb.  The  right 
anterior  limb  likewise  becomes  innervated  through  the  commissural 
fibres  which  connect  the  nuclei  of  origin  of  its  nerves  with  those  of 
the  nerves  of  the  left  posterior  extremity.  All  the  limbs  of  the  dog, 
therefore,  become  innervated  from  one  hemisphere  when  the  other 
hemisphere  is  injured,  so  that,  although  disease  of  one  hemisphere 
causes  a  certain  amount  of  paresis,  no  true  paralysis  or  hemiplegia 
results  as  in  the  case  of  man.  This  condition  has  often  been  induced 
by  experimental  lesions  of  one  of  the  hemisplieres  in  the  dog,  and  it  is 
always  associated  with  conjugate  deviation  of  the  head  and  eyes,  show- 
ing that  both  phenomena  are  induced  by  disease  of  the  same  mechanism. 
But  although  the  dog  does  not  manifest  complete  paralysis  of  the  mus- 
cles of  the  side  opposite  the  lesion — say  the  right  side,  the  lesion  being 
in  the  left  hemisphere — yet,  on  standing,  a  slight  degree  of  pressure  on 
the  left  side  pushes  the  animal  over  to  the  right,  the  vertebral  column  is 
arched  with  the  convexity  towards  the  right,  showing  a  predominance 
of  the  action  of  the  left  erector-spin^  over  their  antagonists,  and  the 
eyes  and  head  are  rotated  to  the  left,  a  position  whicli  indicates  paresis 
of  the  muscles  which  produce  rotation  of  them  to  the  right.  Under 
these  circumstances,  Avhen  the  dog  endeavors  to  advance  he  begins  to 
move  round  his  tail,  a  movement  which  has  been  called  "  mouvement 
de  manege^'  and  Avhich  is  the  equivalent  of  hemiplegia  in  man.  It  is, 
therefore,  probable  that  some  of  the  compulsory  movements  described 
as  automatic  kinesioneuroses  really  belong  to  the  synkineses,  as  at 
present  defined. 

(6)  Disorders  of  the  Associated  Movements  of  Articulation. 

But  when  the  muscles  which  are  bilaterally  associated  in  their  action 
are  small,  and  when  minor  nervous  discharges  only  are  re(i[uisite  to 
throw  them  into  action,  the  connection  of  the  muscles  of  the  two  sides 
with  one  hemisphere  may  be  brought  into  such  habitual  use  that  the 
connection  with  the  other  hemisphere,  although  still  existing,  is  held 
practically  in  abeyance.  The  muscles  concerned  in  executing  the 
movements  of  articulation,  for  instance,  are  bilaterally  associated ;  the 
necessary  adjustments  demand  great  delicacy  of  execution,  but  no  great 
muscular  exertion  ;  the  muscles  engaged  in  executing  the  most  delicate 


192  GENEEAL    SYMPTOMATOLOGY. 

of  these  adjustments  are  small,  and  consequently  these  muscles  fulfil 
all  the  conditions  just  mentioned. 

It  is  now  a  matter  of  almost  daily  observation  that  the  muscular 
adjustments  concerned  in  articulate  speech  are  regulated  from  the  left 
hemis[)here ;  but  it  by  no  means  follows  that  the  regulation  of  all  the 
functions  performed  by  these  muscles  is  similarly  restricted.  The  con- 
tractions of  the  laryngeal  muscles  concerned  in  vocalization,  for  instance, 
are  not  necessarily  interfered  with,  because  the  delicate  adjustments 
required  in  articulate  speech  are  abolished ;  hence  complete  loss  of  the 
power  of  articulate  speech  is  perfectly  compatible  with  entire  absence 
of  voluntary  paralysis  of  any  of  the  muscles  engaged  in  articulation. 
It  is  not  the  power  of  producing  voluntary  contractions  of  these  mus- 
cles which  is  lost,  but  the  power  of  producing  highly  complex  coml)i- 
nations  of  these  contractions.  If  we  suppose  that  v  and  v'  are  the 
spinal  nuclei  of  the  nerves  {v  n,  v  n')  which  supply  the  muscles  of 
articulation,  the  two  nuclei  are  practically  fused  into  one  by  transverse 
commissural  fibres  {c") ;  and  consequently  impulses  which  start  from 
the  left  cortex  (C),  and  pass  through  the  fibres  (3')  to  the  spinal 
nucleus  {v)  of  the  right  side,  readily  reach  the  left  nucleus  (y')  through 
the  commissural  fibres  [c").  But  as  the  muscles  concerned  in  articu- 
lation act  always  bilaterally  and  symmetrically,  the  channels  of  com- 
munication between  the  spinal  nuclei  of  their  nerves  and  the  cortex  of 
one  hemisphere  are  brought  into  habitual  use ;  while  tlie  channels  of 
communication  between  these  nuclei  and  the  opposite  hemisphere 
become  partially  obliterated  from  disuse,  and  prol)ably  not  thoroughly 
developed  from  the  first.  The  channels  of  comnmnication  between  the 
right  cortex  (C)  and  the  nuclei  v  and  v',  for  instance,  are  represented 
by  the  dotted  line  (3  3),  and  the  commissural  fibres  which  convey 
impulses  from  the  left  to  the  right  nucleus  by  the  dotted  line  {c"),  in 
order  to  indicate  that  these  channels  are  only  partially  open.  De- 
struction of  the  communication  (3')  between  the  left  cortex  (C)  and 
the  right  nucleus  {v)  is  followed  by  loss  of  articulate  speech,  a  condition 
Avhich  is  called  aphasia. 

If  the  lesion  destroy  the  portion  of  the  cortex  of  the  left  liemisphere 
—the  posterior  part  of  the  third  frontal  convolution— from  which  the 
fibres  of  communication  spring,  this  condition  is  permanent,  except 
perhaps  in  young  people,  in  whom  the  corresponding  part  of  the  right 
hemisphere  becomes  educated  and  develoi)ed  for  the  purpose.  But  if 
the  lesion  involve  only  the  channel  of  communication  (3')  between  the 
left  cortex  and  the  right  nucleus,  the  loss  of  speech  is  only  temporary. 
The  corpus  callosum  consists  of  fibres  {c  c)  which  connect  symmetrical 
parts  of  the  two  hemispheres;  and  the  portion  of  it  which  connects 


THE    EXTERNAL    KINESIONEUROSES.  193 

the  third  frontal  convolution  of  the  two  sides  is  represented  in  Fig.  72 
by  the  dotted  line  to  show  that,  although  the  connection  exists  it  is 
l)artially  closed  through  disuse.  When,  however,  the  communication 
through  (3')  is  interrupted,  impulses  generated  in  the  third  left  frontal 
convolution  make  their  way  through  the  fibres  of  the  corpus  callosum 
to  the  corresponding  part  of  the  right  hemisphere,  and  after  a  time 
through  the  dotted  line  (8)  which  connects  the  latter  with  the  left 
nucleus,  and,  after  another  interval,  through  the  partially  open  com- 
missural fibres  Avhicli  connect  the  left  (v)  with  the  right  nucleus  (v').  so 
that  the  power  of  speech  is  gradually  reac(|uired.  A  lesion,  however, 
which  destroys  both  the  channel  of  communication  (3')  between  the 
third  left  frontal  convolution  and  the  spinal  nuclei,  and  the  fibres  of 
the  corpus  callosum  [a  r,  dotted  line)  connecting  tlie  right  and  left  third 
frontal  convolutions,  Avill  influence  speech  as  powerfully  and  perma- 
nently as  disease  of  the  gray  substance  of  the  third  left  frontal  convo- 
lution itself.  Such  a  lesion  effectually  cuts  off  the  third  left  frontal 
convolution,  in  which  the  higher  mechanism  which  regulates  the  mus- 
cular adjustments  concerned  in  articulation  is  organized,  from  the  spinal 
nuclei ;  and  the  only  means  by  which  speech  can  be  then  restored  is 
the  organization  of  a  new  mechanism  in  the  corresponding  part  of  the 
right  hemisphere,  a  method  which  must  always  be  slow,  and  which  can 
onh^  take  place,  at  least  to  any  considerable  extent,  in  the  plastic  tissues 
of  young  people. 


13 


CHAPTER  YII. 

GENERAL  SYMPTOMATOLOGY  [contmued). 

II.  The  Visceral  Kinesioneuroses. 

The  motor  affections  of  internal  organs  present  many  peculiarities 
in  comparison  with  those  of  the  organs  of  external  relation.  These 
peculiarities  depend  in  great  part  upon  the  fact  that  the  muscular 
apparatus  of"  the  internal  organs  is  formed  of  unstriated  muscular 
tissue,  which  differs  from  the  striated  muscle  in  its  mode  of  contraction, 
and  in  several  other  respects.  An  unstriated  muscular  fibre  does  not 
respond  to  mechanical  and  electrical  stimuli  by  a  prompt  contraction  of 
short  duration,  but  a  long  latent  period  precedes  the  contraction,  which 
itself  lasts  for  a  considerable  time,  while  relaxation  takes  place  only  in 
a  slow  and  gradual  manner.  Another  peculiarity  of  the  contractions 
of  unstriated  muscles  is  the  rhythmic  and  automatic  manner  in  which 
they  occur ;  these  characteristics  being  well  exemplified  by  the  peri- 
staltic action  of  the  intestines  and  ureters.  It  is  very  ])robable  that 
these  movements  depend  upon  the  presence  of  local  ganglia  on  the 
walls  of  the  organs,  although  there  are  not  wanting  facts  to  show  that 
the  power  of  undergoing  such  contractions  is  an  inherent  property  of 
the  unstriated  muscular  fibres  themselves.  The  functions  of  these 
intramural  ganglia  are  regulated  by  means  of  accelerating  and  retard- 
ing nerve  fibres  from  centres  situated  in  the  cerebi'O-spinal  system,  so 
that  arrest  of  the  contractions  of  unstriated  muscles  may  be  caused  by 
a  destructive  lesion  of  the  accelerator  or  an  irritative  lesion  of  the  in- 
hibitory fibres,  while  spasm  may  be  caused  by  an  irritative  lesion  of 
accelerator  fibres  or  a  destructive  lesion  of  inhil)itory  fibres. 

The  movements  of  the  internal  organs  are  regulated  chiefly  by  the 
ganglia  and  plexuses  of  the  sympathetic  system,  but  these  are  so  inex- 
tricably connected  with  the  cerebro-spinal  system  that  it  is  impossible 
to  draw  any  line  of  demarcation  between  the  two  nervous  mechanisms. 

The  sympathetic  system  of  nerves  consists  of  a  vertebral  and  pre- 
vertebral portion.  The  vertebral  portion  is  composed  of  a  series  of 
ganglia,  united  by  a  longitudinal  cord  (Fig.  78,  I C  to  C)  which  de- 
scends along  each  side  of  the  vertebral  cofumn  from  the  head  to  the 
coccyx.     The  prevertebral  portion   consists  of  the  numerous  ganglia 


THE    VISCEEAL    KINESIOXEUEOSES. 


195 


Superior  Cervical  Ganglion  of  the  Sympathetic:   its  connections  andbrakciies. 
(Reduced  from  Flower.) 
IC  to  IVC,  Branches  of  communication  to  four  upper  cervical  nerves 
PS,  "  "  petrosal  ganglion. 

Vr,  "  "  ganglion  of  root  of  pneumogastric. 

V',  "  "  ganglion  of  trunk  of  pneumogastric. 

H,  "  "  hypoglossal  nerve. 

CP,  Carotid  plexus. 
C'P,  Cavernous  plexus. 

CA,  Branches  accompanying  internal  carotid  artery. 
OG,         "  to  ophthalmic  ganglion. 


X96  GENEEAL    SYMPTOMATOLOGY. 

Ih,  To  tympanii;  branch  of  glosso-pbaryngeal.  g| 

3,  to  third  nerve.  - 

4,  to  fovirth  nerve. 

5,  to  fifth  nerve. 

e,  to  sixth  nerve.  ^ 

V,  Vidian  nerve  to  spheno-palatine  ganglion.  '' 

S  p,  Large  superficial  petrosal  from  facial  nerve. 
E.\0,  Accompanying  branches  of  external  carotid  artery. 

PP    Pharyngeal  plexus,  formed  by  union  with  branches  of  vagus  and  glosso-pbaryngeal  nerves. 
SG,  Superior  cardiac  nerve. 

The  Middle  Ceritical,  or  Thyroid  Ganglion. 
IVC  to  VIC,  Branches  of  communication  with  fourth,  fifth,  and  sixth  cervical  nerves. 
IT,  Inferior  thyroid  branches. 
MC,  Middle  cardiac  nerve. 
RL,  To  recurrent  laryngeal. 

The  Inferior  Cervical  Ganglion. 

VIIC  to  Vine,  Branches  of  communication  with  seventh  and  eighth  cervical  nerves. 
IC,  Inferior  cardiac  nerve. 
CP,  Cardiac  plexus. 
GW,  Ganglion  of  Wrisberg. 
LCP,  Posterior,  or  left  coronary  plexus. 
KCP,  Anterior,  or  right  coronary  plexus. 

CRL,  Cardiac  branches  from  pneumogastric  or  recurrent  laryngeal  nerves. 

APP,  To  right  anterior  pulmonai-y  plexus. 

LPP,  To  left  anterior  pulmonary  plexus. 
ID  to  IID,  Branches  of  communication  from  the  first  to  the  twelfth  doi-sal  nerves. 
a,  a,  To  aorta,  vertebrae,  cesophagus,  and  posterior  pulmonary  plexus. 
GSN,  Great  splanchnic  nerve. 
SSN,  Small  splanchnic  nerve. 
SSN',  Smallest  splanchnic  nerve. 
D,  Diaphragm. 
PN,  Phrenic  nerve. 
SP,  Epigastric,  or  solar  plexus. 

CLP,  ('celiac  plexus. 

Cs,  Cystic  plexus. 

GSD,  Gastro-duodenal  plexus. 

C  s  P,  Gastric  or  coronary  plexus. 

Vy,  Pyloric  plexus. 

SpP,  Splenic  plexus. 

LGsE,  Left  gastro-eplploic  plexus. 

Po-,  Pancreatic  plexus, 

HjjP,  Hepatic  plexus. 

V",  Branches  from  pneumogastric. 

DmP,  Diaphragmatic  plexus. 

SG,  Semilunar  ganglion. 

SK«P,  Suprarenal  plexus. 

BkP,  Renal  plexus. 

SpV,  Spermatic  plexus. 
SMP,  Superior  mesenteric  plexus. 

Mce,  Middle  colic. 

Kce,  Right  colic. 

Ice,  Ileo-colic. 
AP,  Aortic  plexus. 

IMP,  Inferior  mesenteric  plexus. 

LCI,  Left  colic  plexus. 

Sz,  Sigmoid  plexus.  I 

SHni,  Superior  hemorrhoidal  plexus.  I 

IL  to  VL,  Branches  of  communication  with  the  five  lumbar  nerves. 


IS  to  VS, 


five  sacral  nerves. 


IHP,  Pelvic,  or  inferior  hypogastric  plexus,  giving  branches  to  all  the  pelvic  visceni. 


' '       coccygeal  ner\'e. 
HP,  Hypogastric  plexus. 


THE    VISCERAL    K INESIONEUROSES. 


197 


and  plexuses  of  the  head,  chest,  abdomen,  and  pelvis.  The  cerebro- 
si)inal  nerves  communicate  with  the  cord  of  the  sympathetic  at  their 
exit  from  the  cranium  and  vertebral  canal.  The  fourth  and  sixth 
cranial  nerves  communicate  with  the  sympathetic  in  the  cavernous  sinus 
tlie  olfactory  in  the  nose,  and  the  auditory  in  the  meatus  auditorius 
internus.  The  sympathetic  branches  of  distribution  accompany  the 
arteries,  so  that  all  the  organs  of  the  body  are  supplied  by  sympathetic 


nerves. 


1.  Disorders  of  the  Nervous  Mechanism  of  the  Iris  and  other 
Associated  Mechanisms. 

The  nervous  mechanism  of  the  iris  (Fig.  74)  consists  of  a  (1)  con- 
tractor centre  in  the  crus  cerebri  (C),  which  forms  part  of  the  nucleus 


A  A,  psychical  impression  ;  B,  centrum  optici ;  C,  oculo-motor  centre  ;  D,  dilator  centre  (spinal) ;  E, 
iris  ;  G,  optic  nerve  ;  H,  oculo-motor  (sphincter) ;  I,  sympathetic  (dilator) ;  K,*L,  anterior  roots ;  M  N  0, 
posterior  roots;  /^,  seat  of  lesion  causing  reflex  pupillary  immobility  ;  *,  probable  seat  of  lesion  causing 
myosis.     (After  Erb.) 

of  the  third  nerve ;  (2)  a  cortical  contractor  centre  (A),  situated  prob- 
ably in  the  angular  gyrus ;  (3)  a  dilator  centre  in  the  medulla  (D) ; 
and  (4)  a  cortical  dilator  centre  (A),  situated  probably  in  the  posterior 
part  of  the  first  frontal-  convolution.  The  cortical  centres  are  connected 
with  the  contractor  and  dilator  spinal  centres  by  centrifugal  fibres  which 
descend  in  the  pyramidal  tract ;  the  spinal  contractor  centre  is  con- 


198  GENERAL    SYMPTOMATOLOGY. 

nected  with  the  sphincter  of  the  iris  (E)  by  efferent  fibres  (H)  which 
pass  in  the  third  nerve ;  and  the  dilator  nucleus  with  the  dilator  muscle 
by  means  of  efferent  fibres  which  descend  in  the  cervical  region  of  the 
cord,  emero-e  along  with  the  anterior  roots  of  the  eighth  cervical  (K) 
and  first  dorsal  (L)  nerves,  ascend  in  the  cervical  sympathetic,  and 
ultimately  find  their  way  to  the  dilator  fibres  through  the  cavernous 
plexus,  the  lenticular  nucleus,  and  the  ciliary  nerves.  The  contractor 
nucleus  is  connected  with  the  surface  by  afferent  fibres  which  pass  from 
the  retina  (F)  in  the  optic  nerves  and  tracts  (G)  to  the  corpora  quadri- 
gemina  (B),  and  then  bend  down  to  join  the  contractor  nucleus  in  the 
floor  of  the  aqueduct  of  Sylvius.  The  afferent  and  efferent  fibres  of 
the  contractor  nucleus  form  a  reflex  loop,  so  that  when  light  falls  on 
the  back  of  the  eye  the  iris  contracts.  The  dilator  nucleus  appears  to 
be  connected  with  the  surfiice  of  the  body  generally  by  afferent  fibres 
(M  N  0),  so  that  strong  irritation  of  any  part  of  the  surface  of  the 
body  causes  the  iris  to  dilate.  It  will  be  seen  that  only  part  of  this 
mechanism  belongs  to  the  sympathetic  system,  but  it  will  conduce  to 
clearness  if  all  the  disorders  of  the  })U])ils  are  considered  in  this  place. 

The  cervical  sympatlietic  also  contains  vaso-motor  fibres  for  the 
corresponding  half  of  the  head,  and  trophic  and  secretory  fibres  for 
the  salivary  glands.  The  orbital  muscles  of  iSIiiller  are  also  innervated 
from  the  cervical  sympathetic.  Irritation  of  the  fibres  supplying  these 
muscles  causes  the  eyeball  to  protrude  (exophthalmos),  and  the  jialpe- 
bral  aperture  is  consequently  widened ;  while  paralysis  of  them  allows 
the  eyeball  to  fall  back  into  the  orbit,  and  the  palpel)ral  aperture  is 
then  narrowed.  The  eyeball  appears  also  to  undergo  trojihic  change, 
which  increases  the  intraocular  pressure  and  renders  the  cornea  more 
convex  in  irritation  of  the  fibres,  and  diminishes  the  intraocular  pres- 
sure and  renders  the  cornea  flatter  in  paralysis  of  the  fibres. 

a.  Disorders  of  the  Movements  of  the  Iris. 

The  disorders  of  the  movements  of  the  iris  may  be  divided  into  the 
following  varieties,  namely,  (1)  contraction  of  tlie  pupil,  or  myosis  ; 
(2)  dilatation  of  the  pupil,  or  mydriasis ;  (3)  immobility  of  the  pupil 
with  normal  size ;  (4)  clonic  spasm  of  the  muscles  of  the  iris  ;  and  (5) 
reflex  disorders  of  the  pupil. 

(1)  Myosis.— Three  forms  of  myosis  may  be  distinguished,  namely, 
(a)  spastic  or  spasmodic  myosis  caused  by  spasm  of  the  sphincter ; 
{h)  paralytic  myosis,  caused  by  paralysis  of  the  dilator  fibres ;  and 
(c)  combined  spasmodic  and  paralytic  myosis,  caused  bv  simultaneous 
spasm  of  the  sphincter  and  paralysis  of  the  dilator  fibres.     In  the  first 


THE    VISCERAL    KINESIONEUROSES .  199 

two  of  these  varieties  the  i)upil  is  in  a  medium  degree  of  contraction 
and  movable,  and  consequently  they  may  be  named  the  medium  or 
labile  mijoses.  In  the  last  of  the  three  the  pupil  is  in  the  hio-hest 
degree  of  contraction  and  immovable,  and  conse(|uently  it  may  be 
named  maximum  or  stabile  mi/osis. 

(a)  Spastic  myosis,  if  in  high  degree,  prevents  the  pupil  contracting 
to  light  or  during  efforts  at  accommodation.  The  pupil  does  not  dilate 
by  shading  the  eyes,  but  a  moderate  degree  of  dilatation  is  caused  bv 
all  excitants  of  the  dilator  centres  or  fibres,  such  as  a  strong  sensory 
impression  or  emotional  disturbance.  A  minimum  dilatation  is  produced 
by  mydriatics,  and  a  maximum  contraction  by  myotics. 

{b)  Paralytie  nii/osis  does  not  prevent  the  pupil  contracting  to  the 
stimulus  of  light  or  during  efforts  at  accommodation,  but  dilatation 
does  not  occur  in  irritation  of  the  dilator  centres  or  fibres.  A  medium 
degree  of  dilatation  is  produced  by  mydriatics  and  a  maximum  contrac- 
tion by  myotics.  The  pupil  is  more  contracted,  as  a  rule,  in  spas- 
modic than  in  paralytic  myosis. 

(c)  Combined  spastic  and  paralytic  myosis  causes  a  maximum  de- 
gree of  contraction  of  the  pupil,  which  is  also  completely  immovable  to 
the  stimulus  of  light  and  accommodation,  as  well  as  to  those  which  act 
on  the  dilator  centres  and  fibres.  Mydriatics  cause  a  medium  degree 
of  dilatation,  but  myotics  have  no  effect  on  the  size  of  the  pupil. 

(2)  Mydriasis. — Three  forms  of  mydriasis  may^  also  be  distinguished, 
namely,  {a)  spastic  or  spasmodic  mydriasis,  (b)  paralytie  mydriasis, 
(e)  combined  spasmodic  and  paralytic  mydriasis.  In  the  spastic  and 
paralytic  form  the  pupil  is  in  a  medium  degree  of  dilatation,  and 
movable  to  certain  stimuli,  and  conse(piently  they  may  be  named 
medium  or  labile  mydriasis ;  while  in  the  combined  form  it  is  in  a  con- 
dition of  maximum  dilatation  and  immovable,  and  consequently  it  may 
be  called  maximum  or  stabile  mydriasis. 

(a)  Spasinodic  mydriasis  is  characterized  by  a  medium  degree  of 
dilatation  of  the  pupil,  which  contracts  slightly  to  light  and  during 
efforts  at  acconnnodation,  but  does  not  dilate  on  irritation  of  the  dilator 
centre  either  through  sensory  nerves  or  psychical  impressions.  The 
pupil  is  difficult  to  contract  by  myotics,  but  a  maximum  dilatation  is 
readily  produced  by  mydriatics. 

{b)  Paralytic  mydriasis  is  characterized  by  a  medium  degree  of  dila- 
tation of  the  pupil,  which  fails  to  contract  to  the  stimulus  of  light  or 
during  efforts  at  accommodation,  but  dilates  further  on  sensoi-y  or 
psychical  irritation  of  the  dilator  spinal  centre.  A  maximum  dilatation 
is  readily  produced  by  mydriatics,  but  a  medium  contraction  alone  is 
produced  by  myotics. 


200  GENEllAL    SYMPTOMATOLOGY. 

((•)  Oomhined  spasmodic  and  'paralytic  mydriasis  is  cliaructerized  by 
the  pupil  being  in  a  maxinium  degree  of  dilatation,  and  eorai)letely 
reactionle.ss  to  all  kinds  of  stimuli.  It  is  not  possible  to  ol)tain  a 
further  dilatation  of  the  pupil  by  mydriatics,  but  a  medium  degree  of 
contraction  is  produced  by  myotics. 

(8)  Complete  immohllity  of  the  pupil  with  normal  size  is  caused  by 
paralysis  of  both  the  dilator  and  contractor  muscles  of  the  iris.  When 
the  muscles  of  the  iris  are  alone  affected  the  condition  is  named  (<i)  Iri- 
doplegia,  but  when  all  the  internal  muscles  of  the  eye  are  paralyzed 
the  condition  is  named  (b)  ophthalmoplegia  interna. 

(a)  Tridoplci/ia  is  characterized  by  the  pupil  being  midway  between 
dilatation  and  contraction,  and  being  innnovable  to  every  form  of 
stimulus.  Hutchinson  states  that  the  power  of  being  acted  upon  by 
myotics  and  mydriatics  is  only  completely  lost  Avhen  the  substance  of 
the  iris  itself  is  disorganized. 

(b)  Ophthalmoplegia  interna  is  characterized  by  the  pupil  being 
midway  between  dilatation  and  contraction,  and  completely  reactionless, 
while  in  addition  the  power  of  acconnnodation  to  near  vision  is  lost. 

(4)  Clonic  spaf<m  of  the  inuseles  of  the  ii'is  is  named  hippus  or 
chorea  of  the  iris;  it  consists  of  (juickly  alternating  contractions  and 
dilatations  of  the  pupil,  which  depend  probably  upon  a  clonic  spasm  of 
the  sphincter.  It  sometimes  accompanies  nystagnms,  while  at  other 
times  it  is  observed  during  the  regressive  period  of  paralysis  of  the 
third  nerve. 

(5)  Disorders  of  the  reflex  movements  of  the  iris  may  be  divided 
into  those  of  (a)  the  irido-dilator,  and  (6)  the  irido-contr actor  reHex  arc. 

{a)  Disorders  of  the  irido-dilator  reflex  arc  may  be  subdivided  into 
those  caused  l)y  lesion  (j)  of  the  efferent  and  ( jj)  of  tlie  afferent  por- 
tion of  the  reHex  arc. 

(j)  Disorder  of  the  efferent  portion  of  the  reflex  dilator  arc  is  met 
with  in  locomotor  ataxia.  A  strong  sensory  irritation  of  any  part  of 
the  body  is  followed  in  healthy  persons  ])y  dilatation  of  the  i)U])ils,  but 
this  reaction  fails  to  take  place  in  many  cases  of  locomotor  ataxia,  the 
reflex  arc  being  interrupted  by  lesion  of  the  efferent  fibres  of  the 
ddator  centre  in  their  descending  course  through  the  cervical  portion  of 
the  cord. 

(jj)  Disorder  of  the  Aferent  Portion  of  the  Reflex  Dilator  Are. — 
When  there  is  complete  anaesthesia  of  the  lower  part  of  the  hotly  from 
spinal  disease,  irritation  of  the  anesthetic  area  is  not  followed  by  dilata- 
tion of  the  pupils,  but  in  cerebral  anaesthesia,  simulated  anesthesia,  and 
probably,  also,  in  hysterical  anagsthesia,  the  reaction  is  not  interfered 


I 


THE    VISCERAL    KINESIONEU  ROSES.  Wl 

Avitli.  This  reaction,  tlicrefoiv,  may  be  found  a  useful  test  in  distin- 
<^uis]iing  spiiuil  anesthesia  from  the  other  forms. 

(b)  Disorders  of  the  irido-rontractor  rcjlcx  arc  may  he  di\ided  into 
those  which  are  caused  by  disease  of  (j)  the  efferent  fibres  of  the  arc 
which  pass  in  the  third  nerve,  the  short  root  of  the  lenticuhir  fan^rlion, 
and  the  ciliary  nerves;  (jj)  the  afferent  fibres  of  the  arc,  which  pass 
from  the  retina  through  the  optic  nerves  and  tracts  to  the  corpora 
((uadrigemina;  and  (jjj)  the  loop  which  joins  the  corpoi-a,  ((uadrigemina 
with  the  nucleus  of  tlie  third  nerve. 

(j)  Disordn-  of  the  ^ffererit  Portion  of  the  Irido-contraetor  llejit'x 
Arc. — When  the  j)upil  fails  to  react  to  the  stimulus  of  light  from  lesion 
of  the  eflerent  fibres  of  the  reflex  arc,  the  sphincter  of  the  iris  is  found 
to  be  paralyzed,  and  the  other  symptoms  which  indicate  partial  or  com- 
plete paralysis  of  the  third  nerve  are  generally  present. 

(jj)  Disorder  of  the  Afferent  Portion  of  the  Irido-contr actor  Reflex 
Arc. — In  atrophy  Avith  blindness  of  the  optic  nerves  the  sphincters  of 
the  iris  lose  their  tone,  and,  provided  the  sympathetic  mechanism  be 
free  from  disease,  the  pupils  dilate,  and  they  fail  to  contract  to  the 
stimulus  of  light,  Init  still  retain  the  power  of  contracting  when  the 
eyes  are  converged.  In  unilateral  atrophy  with  blindness  both  pupils 
fail  to  contract  when  light  is  admitted  to  the  affected  side,  but  both 
contract  readily  when  light  is  admitted  to  the  sensitive  eye,  because 
the  central  cord  of  the  contractor  reflex  arc  is  coimected  with  its  fellow 
of  tiie  opposite  side  by  commissural  fibres.  In  blindness  from  a  lesion 
situated  above  the  corj)ora  quadrigemina,  contraction  of  the  pupil  to 
light  is  retained,  because  the  reflex  arc  is  unaflected  and  consecpiently 
the  presence  or  absence  of  reflex  contraction  of  the  pupil  to  light  in 
cases  of  blindness  is  a  valuable  diagnostic  sign  in  determining  the 
localization  of  the  lesion. 

(jjj)  Reflex  Dmiiohility  of  the  Pupil  {the  Argyll- Robertson  Pupil). 
— In  this  condition  there  is  absence  of  reflex  contracticm  of  the  pupil 
to  lifiht,  while  the  associated  contraction  with  accommodation  is  re- 
tained,  and  vision  may  be  normal.  The  absence  of  any  paralysis  of 
the  sphincter  and  of  blindness,  shows  that  the  efferent  and  afferent 
fibres  of  the  reflex  ai-c  are  unaffected,  and  consequently  the  lesion  must 
be  situated  in  the  fibres  which  connect  the  corpora  quadrigemina  with 
the  nucleus  of  the  third  nerve  (Fig.  75);  the  interruption  taking  place 
most  probably  near  the  descending  root  of  the  fifth  nerve.  This  symp- 
tom is  met  Avith  almost  exclusively  in  locomotor  ataxia  and  general 
paralysis  of  the  insane. 


202  GENEKAL    SYMPTOMATOLOGY. 

b.  Disorders  of  the  Vaso-motor  and  Other  Mechanisms  or  the  Cervical 
Sympathetic  and  Cilio-spinal  Kegion  of  the  Spinal  Cord. 

The  symptoms  caused  bv  disease  of  the  cervical  portion  of  the  sym- 
pathetic differ  according  as  the  lesion  is  (1)  an  irritative  or  (2)  a  de- 
pressive one. 

(1)  Irritative  Phenomena. — When  the  sympathetic  centres  in  the 
medulla  oblongata,  or  the  efferent  fibres  -which  connect  them  with  the 
periphery,  are  irritated,  the  pupil  becomes  dilated  (spasmodic  mydri- 
asis) ;  the  palpebral  aperture  is  increased  in  size ;  the  eyeball  becomes 
slightly  protruded  (exophthalmos) ;  the  temporal  artery  is  contracted, 
and  feels  like  a  hard  cord  under  the  finger ;  the  skin  of  the  half  of  the 
face  and  the  ear  on  that  side  is  pale  and  cold  to  the  touch  ;  and  the 
temperature  in  the  external  meatus,  and  probably  in  the  cavities  of  the 
mouth  and  nose  on  that  side,  is  lowered  as  compared  with  that  on  the 
opposite  side.  The  phenomena  of  irritation  of  the  sympathetic  are 
somewhat  transient,  so  that  we  do  not  possess  any  very  accurate  infor- 
mation with  regard  to  the  state  of  the  secretions  in  such  cases ;  but  I 
have  observed,  in  cases  of  cervical  pachymeningitis  with  dilated  pupils, 
that  the  face  has  often  an  oily  appearance,  as  if  the  secretion  of  sweat 
were  not  so  much  increased  in  (piantity  as  altered  in  quality.  There 
are  no  very  accurate  observations  with  regard  to  the  condition  of  the 
secretion  of  tears,  saliva,  or  of  that  from  tlie  mucous  membrane  of  the 
nose. 

(2)  Depressive  Pheno)nena. — When  the  sympathetic  centres  in  the 
medulla,  or  the  fibres  which  connect  tliem  with  the  periphery,  are 
paralyzed,  the  pupil  is  contracted  (paralytic  myosis) ;  the  intraocular 
tension  is  diminished  and  the  cornea  flattened ;  the  eyeball  is  retracted 
or  falls  back  into  the  orbit,  and  its  pressure  against  the  eyelids  being 
thus  lessened,  the  palpebral  fissure  becomes  narrower ;  the  temporal 
artery  is  dilated  and  tortuous ;  the  skin  of  the  face  and  side  of  the 
head  on  the  affected  side  may  be  congested,  especially  at  first ;  the 
temperature  in  the  external  meatus,  the  mouth,  and  the  nostril  is  in- 
creased on  the  diseased  as  compared  with  corresi)onding  ])arts  on  the 
healthy  side ;  and  the  secretions  of  tears,  saliva,  and  sweat,  as  well  as 
that  from  the  mucous  membrane  of  the  nose,  are  diminished  on  tlie 
side  of  the  lesion ;  while  the  skin  of  the  face  looks,  in  long-standing 
cases,  more  flabby  and  wrinkled  and  older  than  tliat  of  the  opposite 
side.  When  the  disease  has  become  chronic,  the  vessels  on  the  affected 
side  of  the  face  may  cease  to  be  dilated ;  and  when  the  patient  exerts 
himself  so  that  the  cutaneous  vessels  of  the  bodv  generally  become 
ddated,  the  healthy  side  of  the  face  becomes  flushed  and  covered  with 


THE    VISCERAL    KIXESIONEU  ROSES.  203 

perspiration,  while  the  aftected  half  retains  its  normal  appearance  and 
remains  free  from  moisture.  The  diseased  side  may  also  remain  dry 
when  the  patient  takes  a  hot  bath.  Bilateral  paralysis  of  the  sympa- 
thetic centres  in  the  medulla  oblongata,  such  as  sometimes  occurs  in 
progressive  muscular  atrophy,  is  attended  by  a  great  flow  of  viscid 
saliva  corresponding  to  the  paralytic  secretion  obtained  by  experiments 
on  animals. 

Morbid  Anatonry  and  Physiology. — Organic  lesions  of  the  sympa- 
thetic may  be  divided  into  those  which  implicate  (1)  the  centres  in  the 
medulla  oblongata  or  the  conducting  fibres  in  their  descending  course 
through  the  cervical  portion  of  the  spinal  cord  (Fig.  74,  D  to  K,  L) : 
and  (2)  the  fibres  in  their  course  through  the  rami  communicantes  of 
the  eighth  cervical  and  first  dorsal  nerves  (Fig.  74,  K.  L)  and  the 
cervical  sympathetic. 

(1)  Lesioxs  of  the  3IeduUa  Oblongata  and  of  tlie  Cervical  Portion 
of  the  Spinal  Cord. — Oculo-pupillary  phenomena  are  not  mentioned  as 
being  present  in  reported  cases  of  lesions  of  the  medulla  oblongata,  but 
a  case  is  under  my  care  just  now  in  which  there  is  decided  paralytic 
myosis  and  diminution  of  the  palpebral  fissure  of  the  right  eye,  and  in 
which  the  accompanying  symptoms  would  seem  to  indicate  that  the 
lesion  is  situated  in  the  medulla.  The  patient  had  an  apoplectic  attack 
four  or  five  weeks  ago,  and  he  is  now  suffering  from  left-sided  hemi- 
plegia and  crossed  hemianaesthesia,  the  right  half  of  the  face  and  the 
left  half  of  the  body  being  anaesthetic.  In  addition,  the  patient  is 
(piite  unable  to  maintain  the  erect  posture,  although  he  is  not  com- 
pletely paralyzed  even  on  the  left  side  of  the  body ;  and  when  he  is 
placed  on  his  legs  between  two  attendants  he  staggers  from  side  to  side, 
and  throws  his  legs  about  in  the  most  irregular  manner  when  he 
attempts  to  move.  The  staggering  and  incoordination  are  most  prob- 
ably caused  by  implication  of  the  fibres  coming  from  the  inferior 
peduncles  of  the  cerebellum.  The  crossed  hemianesthesia  is  likewise 
best  explained  by  supposing  that  the  lesion  is  situated  in  the  medulla, 
causing  simultaneous  injury  of  the  sensory  conducting  paths  in  their 
passage  through  the  medulla,  and  of  the  ascending  root  of  the  fifth 
nerve.  The  excessive  flow  of  saliva  which  is  present  in  advanced  cases 
of  bulbar  paralysis  is  most  probably  caused  by  paralysis  of  the  sym]ia- 
thetic  centres  in  the  medulla  oblongata.  Dilatation  of  both  pupils, 
along  with  paralysis  of  the  four  extremities,  and  a  remarkably  small 
and  slow  pulse  (48  per  minute),  was  observed  by  Rosenthal  in  a  person 
who  had  been  stabbed  in  the  neck  in  the  neighborhood  of  the  sixth 
cervical  vertebra.  Oculo-pupillary  phenomena,  sometimes  of  the  irri- 
tative and  at  other  times  of  the  depressive  variety,  have  been  frequently 


204  GENERAL    SYMPTOMATOLOGY. 

observed  in  cervical  spinal  pachymeningitis  and  in  fractures  of  the 
cervical  spine ;  and  the  fact  that  these  phenomena  are  also  fre(|uently 
present  in  locomotor  ataxia  would  seem  to  indicate  that  the  efferent 
fibres  pass  downwards  through  the  posterior  columns  of  the  cord,  while 
the  absence  of  these  symptoms  from  cases  of  progressive  muscular 
atrophy  and  acute  spinal  atrophic  paralysis  shows  that  the  efferent 
fibres  are  not  likely  to  pass  through  the  gray  anterior  horns. 

(2)  Lesions  of  the  Rami  Coinmunicantes  and  of  the  Cervical 
Sympathetic. — The  rami  communicantes  are  sometimes  implicated  in 
cases  of  cervical  pachymeningitis  as  they  emerge  from  the  spinal  cord 
with  the  anterior  roots  of  the  eighth  cervical  and  first  dorsal  nerves, 
and  in  the  early  stages  of  such  cases  the  irritative  phenomena  may  be 
present,  but  these  soon  give  place  to  the  depressive  symptoms.  The 
rami  communicantes  are  divided  in  cases  of  rupture  of  the  brachial 
plexus,  and  in  these  cases  the  paralytic  oculo-impillary,  vaso-motor, 
and  secretory  phenomena  are  ahvays  well  marked.  These  symptoms 
are  also  frequently  met  with  in  aortic  aneurisms  and  mediastinal  tumors 
from  pressure  on  the  inferior  ganglion  of  the  cervical  sympathetic,  in 
compression  of  the  cervical  sympathetic  from  goitre  and  other  tumors, 
and  in  these  cases  the  irritative  symptoms  may  be  present ;  but  the 
paralytic  plienomena  are  much  more  frequently  met  with.  The  de- 
pressive phenomena  may  also  be  caused  by  division  of  the  cervical 
sympathetic  from  gunshot  wounds.  The  irritative  and  depressive 
phenomena  of  the  sympathetic  are  also  met  with  in  certain  functional 
diseases,  such  as  hemicrania. 

The  explanation  of  these  symptoms  is  to  be  found  in  the  facts,  estab- 
lished by  experiments  on  animals,  that  the  cilio-spinal  region  of  the 
cord  and  the  cervical  sympathetic  contains  not  only  dilator  fibres  for 
the  iris,  but  also  vaso-motor  fibi-es  for  the  bloodvessels  of  the  side  of 
the  face,  and  secretory  fibres  for  the  lachrymal,  salivary,  and  nasal 
secretions.  It  would  also  appear  that  the  cervical  sympathetic  contains 
trophic  fibres  for  the  eyeball,  as,  after  section  of  it,  Brown-Sequard 
found  gradual  atrophy  of  the  eye  to  take  place  on  the  side  operated 
upon.  The  diminution  of  the  intraocular  tension  and  the  flattening  of 
the  cornea  which  occur  in  paralysis  of  the  sympathetic  filjres  in  man  is 
probably  caused  by  lesion  of  these  trophic  fibres.  The  cervical  sympa- 
thetic also  contains  fibres  which  regulate  tlie  contractions  of  the  muscles 
of  Miiller  in  the  orbit ;  and  when  these  fibres  are  irritated  the  muscles 
are  maintained  in  a  state  of  contraction,  and  the  globe  is  protruded ; 
and  when  they  are  paralyzed  the  muscles  relax  and  allow  the  globe  to 
fall  back  into  the  orbit,  and  the  palpebral  fissure  is  diminished. 


THE    VISCERAL    KIXESIOXEU  ROSES . 


205 


2.  Disorders  of  tJc  Ncrvom  Meclianhm  of  the  Heart. 

a.   The  Cardiac  Nervous  Mechanism. 

The  nervous  centres  which  preside  over  the  movements  of  the  heart 
consist  of  intracardiac  ganglia,  centres  in  the  meduHa  oblongata,  and 
centres  in  the  cortex  of  the  brain.  The  positions  of  these  centres  may 
be  illustrated  by  the  annexed  diagram  (Fig.  To).     The  cardiac  muscle 

Fig.  75. 


0'    \e 


(^^     MA 


U  k" 


1 1  !  ^^\- 


I    I    I 


Schema  of  the  Action  of  the  Cardiac  Neevous  Mechanism. 
CA,  intramural  motor  ganglia  of  the  lieart ;  CI,  intramural  inhibitory  ganglia;  MI  and  MA,  centres 
in  the  niedulla  oblongata,  the  former  being  inhibitory,  the  latter  motor;  B,  centre  in  cortex  of  brain  ;  <i, 
afterent  filire  to  intramural  ganglion  cell ;  a',  afiferent-motor  or  excito-motor  tibre ;  a",  afferent  inhibitory 
or  excito-inhibitoi-y  fibre;  a'",  afferent  fibres  connecting  periphery  with  cortex  of  brain;  e',  effero-motor 
fibre ;  e"  and  e'",  effero-inhibitory  fibres  ;  e,  e,  efferent  fibres  of  the  reflex  arc  of  the  motor  intramural 
ganglia ;  c,  c',  fibres  connecting  the  cortex  of  the  cerebrum  with  the  centres  in  the  medulla  oblongata. 
The  arrows  indicate  the  direction  of  the  conduction. 

is  represented  by  H,  and  the  endocardium  by  E  ;  CA  represents  the 
intramural  ganglia ;  MA  and  MI  the  motor  accelerating  and  the  motor 
inhibitory  centres  respectively ;    and   B   the  cortical   centre,  which   is 


206  GENEEAL    SYMPTOMATOLOGY. 

represented  not  only  as  a  motor  centre,  but  also  as  receiving  sensory 
fibres  from  the  heart  and  from  the  periphery  of  the  body.  These  cen- 
tres are  connected  with  the  periphery  and  with  one  another  and  the 
heart  in  various  ways :  Firstly.  Afferent  fibres  (not  represented  in  the 
diao-ram)  connect  the  endocardium  and  the  muscuLar  fibres  with  a  car- 
diac sensory  cortical  centre.  These  fibres  pass  from  the  heart  through 
the  cardiac  plexuses,  and  the  great  cardiac  nerve  to  the  middle  ganglion 
of  the  cervical  sympathetic ;  but  their  subse^juent  course  through  the 
spinal  cord  and  brain  is  not  known.  Irritation  of  these  fibres  in  any 
part  of  their  course  causes  cardiac  pain  or  angina.  Secondly.  Afferent 
fibres  (a')  connect  the  endocardium  Avith  the  intramural  motor  ganglia 
(CA),  and  from  the  latter  issue  fibres  (e)  which  are  distributed  to  the 
cardiac  muscle  (H).  This  constitutes  a  simple  reflex  mechanism. 
Thirdly.  Afferent  fibres  {a")  connect  the  periphery  of  the  body  with 
the  cardiac  accelerator  centre  in  the  medulla,  and  irritation  of  these 
renders  the  action  of  the  heart  more  frequent.  These  fibres  are  called 
excito-motor,  but  affero-accelcratiny  fibres  would  best  characterize  tlieir 
functions.  Fourthly.  Afferent  fibres  (a'")  connect  parts  of  the  peri- 
phery with  the  cardio-inhibitory  centre  in  the  medulla,  and  irritation  of 
these  renders  the  action  of  the  heart  slower.  These  fibres  are  called 
exeito-inhibitory,  but  affero-inhihitory  would  best  characterize  their 
functions.  It  is  possible  that  each  of  the  centres  in  the  medulla  is 
connected  by  afferent  fibres  with  the  endocardium  and  the  muscular 
fibres  of  the  heart,  but  these  are  not  represented  in  the  diagram. 
Fifthly.  Afferent  fibres  {a"")  connect  the  surface  of  the  body,  either 
directly  or  indirectly,  with  the  cortical  motor  centre  (B).  Sixthly. 
Intercentral  fibres  {e')  connect  the  motor  accelerating  centre  (MA)  in 
the  medulla  and  the  intramural  cardiac  ganglia  (CA);  they  convey 
efferent  impulses  which  increase  the  activity  of  the  heart,  and  are  con- 
sequently called  acecleratinji  JihrcH.  Seventhly.  Intercentral  fibres  {e'^ 
and  e'")  connect  the  inhibitory  centre  (MI)  in  the  medulla  and  the 
intramural  ganglia  (CA)  ;  they  carry  impulses  which  arrest  the  action 
of  the  heart,  and  are  therefore  called  cardio-inhibitory  fibres.  Various 
physiological  facts  seem  to  indicate  that  between  the  cardio-inhibitory 
centre  in  the  medulla  (MI)  and  the  intramural  motor  ganglia  (CA) 
intermediate  ganglia  (CI)  are  interposed,  which,  from  their  action,  are 
called  intramural  cardio-inhibitory  ganglia.  Eighthly.  Intercentral 
fibres  (c  and  c')  connect  the  cortex  of  the  opposite  hemisphere  of  the 
brain  with  the  cardio-motor  and  cardio-inhibitory  centres  in  the  me- 
dulla. These  fibres  may  respectively  be  called  centrifugo-motor  and 
centrifugo-inhibitory  fibres. 


THE    VISCERAL    KI  NESIONE  U  ROSES  .  207 

b.  Disorders  of  the  Cardiac  Nervous  Mechanism. 
(1)  disorders  of  the  sensory  nerves  of  the  heart  (angina  pectoris). 

Angina  pectoris  occurs  in  paroxysms  which  are  separated  from  one 
another  by  longer  or  shorter  intervals.  The  attack  begins  by  a  sudden, 
shooting,  tearing,  or  burning  pain,  which  is  felt  at  the  lower  part  of 
the  sternum  and  shoots  over  the  left  side  of  the  chest  and  neck,  or 
along  the  sternum  and  down  the  left  or  botli  arms.  At  the  same  time 
a  feeling  of  oppression  or  constriction  is  felt  across  the  chest,  which  is 
accompanied  by  a  sense  of  suffocation  and  inability  to  breathe.  Dur- 
ing the  paroxysm  the  arteries  feel  like  cords,  and  the  pulse  is  small  and 
wiry,  or  feeble,  irregular,  and  intermittent ;  the  surface  of  the  body  is 
pale  and  cold ;  the  face  is  pale,  sunken,  and  covered  with  sweat ;  and 
tlie  expression  is  one  of  great  alarm  and  fear ;  while  it  has  an  unac- 
countable feeling  of  anxiety  and  fear  of  impending  death.  At  the  end 
of  the  attack  the  pulse  becomes  full  and  soft ;  the  skin  becomes  warm, 
red,  and  covered  with  abundant  perspiration.  The  paroxysm  is  gener- 
ally of  short  duration,  lasting  only  a  few  minutes ;  but  sometimes  the 
attack  is  made  up  of  a  series  of  paroxysms,  each  being  followed  bv  a 
remission  or  a  complete  intermission  of  the  distressing  symptoms.  The 
paroxysms  recur,  as  in  epilepsy,  at  extremely  variable  intervals,  and 
the  course  of  the  disease  is  always  chronic.  The  spinous  and  trans- 
verse processes  of  the  cervical  and  upper  dorsal  vertebrae  and  the  region 
of  the  inferior  angle  of  the  scapula  are  sometimes  tender  to  pressure, 
either  during  the  attacks  or  continuously. 

It  would  appear  that  the  essential  condition  which  underlies  angina 
pectoris  is  loss  of  the  balance  which  ought  to  be  maintained  between 
the  propulsive  powers  of  the  heart  and  the  resistance  to  be  overcome, 
the  conditions  being  altered  in  such  a  way  that  the  muscular  walls  of 
the  heart  are  subjected  to  strain.  This  state  may  result  from  all  con- 
ditions which  weaken  the  muscular  power  of  the  heart,  such  as  the 
auc^mia  caused  by  calcification  of  the  coronary  arteries,  and  fatty 
degeneration  of  its  muscle ;  and  from  all  conditions  which  cause  an 
obstruction  to  the  onward  flow  of  blood,  such  as  aortic  obstruction,  and 
diminution  of  the  calibre  of  the  arterioles  generally,  either  by  disease 
of  their  walls  or  spasm  of  their  muscular  coats.  It  will,  therefore,  be 
apparent  that  the  symptoms  of  angina  will  accompany  many,  probably 
most,  of  the  organic  disorders  of  the  heart. 

(2)  disorders  of  the  simple  reflex  cardiac  mechanism. 

The  heart  may  be  thrown  into  action  after  it  has  been  removed  from 
the  chest  by  stimulating  the  endocardium,  a  fact  which  shows  that  the 


208  GEXEKAL    SYilPTOMATOLOGY. 

afferent  fibres  connect  this  membrane  with  the  intramural  ganglia, 
Avhich  in  their  turn  are  connected  by  efferent  fibres  with  the  muscular 
fibres.  Poisons  which  act  on  the  muscular  substance  of  the  heart,  as 
the  salts  of  potassium,  lactic  acid  and  its  salts,  destroy  this  mechanism 
bv  rendering  the  muscle  incapable  of  responding  to  a  nervous  stimulus. 
Such  poison's  arrest  the  action  of  the  heart  in  diastole.  Landois  has 
shown  that  weak  solutions  of  these  agents,  when  injected  into  the  endo- 
cardium of  the  frog,  stimulate  this  reflex  mechanism,  and  accelerate 
the  action  of  the  heart,  while  stronger  solutions  paralyze  it.  Irrita- 
tion of  this  reflex  mechanism  in  disease  accelerates  the  action  of  the 
heart,  while  all  depressive  influences  upon  it  render  the  action  of  the 
heart  slow  and  feeble,  and  angina  is  found  associated  with  the  last  state. 

(3)    DISORDERS    OF    THE    CARDIO-INHIBITORY    MECHANISM. 

{a)  Disorders  of  the  Inhibitors/  Fibres  of  the  Vagus. — The  beat  of 
the  heart  may  be  checked  or  stopped  in  diastole  by  stimulating  the 
peripheral  part  of  the  divided  vagus  nerve.  The  inhibitory  fibres  (e") 
of  the  vagus  are  paralyzed  by  curara,  the  action  of  the  heart  is  then 
accelerated,  and  is  not  rendered  slow  by  stimulation  of  the  vagus. 
Electrical  stimulation  of  the  sinus  venosus  will,  however,  still  inhibit 
the  cardiac  beats,  and  to  account  for  this  action  the  existence  of  intra- 
mural cardio-inhibitory  ganglia  are  assumed.  Nicotine  stimulates  the 
same  fibres  which  curara  paralyzes  and  consequently  the  action  of 
these  drugs  is  strictly  antagonistic.  But  atropia  paralyzes  the  intra- 
mural inhibitory  mechanism,  while  physostigma  stimulates,  so  tliat 
these  drugs  are  also  antagonistic  in  their  action  on  the  heart.  But 
although  atropia  and  nicotine,  and  curara  and  physostigma  have 
opposite  effects  on  the  cardiac  rhythm,  yet  they  are  not  mutually 
antagonistic.  Atropia  and  physostigma  will  check  the  action  of  nico- 
tine and  curara  respectively,  but  the  latter  drugs  have  no  effect  in 
checking  the  action  of  the  former.  Muscarin  and  jaborandi  produce 
standstill  of  the  heart  which  may  be  removed  by  atropia,  yet  neither  of 
the  former  drugs  has  any  influence  ui)on  the  action  of  the  hitter. 
From  this  it  is  inferred  that  muscarin  and  jaborandi  stinmlate  the 
inhibitory  fibres  of  the  vagus,  but  do  not  affect  the  intranmral  cardio- 
inhibitory  mechanism. 

Irritation  of  the  vagus  is  indicated  by  a  full,  hard,  retjirded  pulse, 
increased  force  of  the  cardiac  beats,  disorders  of  phonation  and  deglu- 
tition, and  sometimes  temporary  arrest  of  the  heart's  action.  Paralysis 
of  the  vagus  is  indicated  by  increased  rapidity  of  the  pulse,  which 
may  beat  as  high  as  from  216  to  240  times  in  a  minute.     This  form  of 


THE    VISCERAL    KIN  ESI  ONEU  ROSES .  209 

accelerated  action  of  the  heart  is  sometimes  associated  with  attacks  of 
bronchial  asthma. 

(b)  Disordci's  of  the  Cardio-inliihitory  Centre  in  the  Medulla. — In 
acute  and  chronic  diseases  of  the  base  of  the  brain  the  rhythm  of  the 
heart  is  greatly  changed,  and  this  is  probably  due  to  irritation  or  paral- 
ysis of  the  cardio-inhilutory  centre  in  the  medulla.  In  tubercular 
meningitis,  for  instance,  the  pulse,  which  is  at  first  very  slow,  becomes 
very  quick  towards  the  terminal  period  of  the  disease.  Great  accelera- 
tion of  the  pulse  is  also  met  with  in  the  various  forms  of  bulbar  paral- 
ysis, and  in  cases  of  locomotor  ataxia  with  gastric  crises  and  other 
symptoms  indicative  of  disease  of  the  medulla. 

[(■)  Disorders  of  the  Reflex-inhihitory  Mechanism. — It  would  appear 
that  powerful  stimulation  of  any  part  of  the  body  will  produce  reflex 
inhibition  of  the  heart.  Crushing  of  a  frog's  foot  will,  for  instance, 
stop  the  cardiac  beats,  and  in  man  the  fainting  which  occurs  during 
severe  pain  is  caused  by  an  inhibitory  action  on  the  heart.  Injury  of 
the  intestines,  however,  appears  to  exercise  a  more  powerful  effect  on 
the  heart  than  that  of  any  other  part  of  the  body.  If  the  abdomen  of 
a  frog  be  laid  bare  and  the  intestines  be  sharply  struck,  the  heart  will 
stand  still  in  diastole,  and  the  same  effect  is  produced  by  strong  stimu- 
lation of  the  mesenteric  nerves,  but  this  action  fails  in  both  cases  if  the 
vagi  are  previously  divided.  Disease  of  the  abdominal  organs  often 
gives  rise,  by  reflex  irritation  of  the  vagi,  to  a  kind  of  angina,  which 
Landois  has  named  angina  pectoris  rejlectoria. 

(4)    DISORDERS    OF    THE    EXCITO-MOTOR   OR   ACCELERATOR   MECHANISM. 

Stimulation  of  certain  parts  of  the  spinal  cord,  and  of  certain  fibres 
of  the  sympathetic,  causes  acceleration  of  the  heart's  action,  but  section 
of  these  nerves  does  not  render  the  action  of  the  heart  slower,  and 
consequently  the  accelerator  and  inhibitory  fibres  are  not  to  be  re- 
garded as  antagonistic,  this  view  being  still  further  confirmed  by  the 
tact  that  simultaneous  stimulations  of  these  fil)res  do  not  neutralize  each 
other.  When  the  accelerating  fibres  are  irritated  bv  disease  the  svmp- 
toms  are  the  same  as  are  caused  by  stimulation  of  the  simple  reflex 
motor  mechanism. 

(5)    ANGINA    PECTORIS    VASO-MOTORIA. 

The  symptoms  of  angina  are  sometimes  caused  by  irritation  of  the 
vaso-motor  nerves,  but  this  condition  will  be  considered  with  the  angio- 
neuroses. 

14 


210  GENEEAL    SYMPTOMATOLOGY. 

3.  Disorders  of  the  Nervous  3Iechanism  of  Respiration. 

a.  The  Kespiratory  Nervous  Mechanism. 

The  nervous  mechanism  of  respiration  consists  of  nerve  centres  and 
their  connection  with  one  another,  with  the  muscles  of  respiration,  and 
with  the  periphery  of  the  body. 

The  respiratory  nerve  centres  are  situated  in  the  spinal  cord  and 
medulla  oblongata,  and  in  the  cortex  of  the  brain.  The  spinal  centres 
are  the  nuclei  of  origin  of  the  thoracic,  phrenic,  and  spinal  accessory 
nerves,  and  to  these  may  be  added  the  nuclei  of  origin  of  the  nasal 
branches  of  the  facial  nerve,  and  of  some  of  the  fibres  of  the  superior 
laryngeal  nerve.  The  respiratory  centres  in  the  medulla  are  situated 
beneath  the  fourth  ventricle,  at  the  nuclei  of  origin  of  the  pneumo- 
gastric  and  spinal  accessory  nerves.  This  centre  controls  and  regu- 
lates the  spinal  centres,  inasmuch  as  destruction  of  it  arrests  all  respira- 
tory movements.  The  cortical  motor  respiratory  centres  appear  to  be 
situated  on  the  internal  surface  of  the  hemisphere.  The  following  are 
some  of  the  conducting  fibres  of  the  respiratory  mechanism  :  Firstly. 
Afierent  fibres  from  the  surface  of  the  body  generally  influence  the  res- 
piratory cortical  centres,  and  consequently  any  sudden  impression  upon 
the  surface  of  the  body  interferes  with  the  resj)iratory  rhythm.  Secondly. 
Afferent  fibres  from  certain  parts  of  the  body  influence  the  respiratory 
centre  in  the  medulla.  Breathing  is  arrested  in  inspiration  by  cold  sud- 
denly applied  to  the  surfjice  of  the  body,  and  it  is  temporarily  arrested 
in  expiration  by  a  sudden  irritation  of  the  mucous  membrane  of  the  nose, 
the  irritation  being  conveyed  through  the  branches  of  the  fifth  nerve. 
Thirdly.  Affero-acerlerating  fibres  to  the  respiratory  centre  are  con- 
tained in  the  trunk  of  the  vagus.  If  tlie  vagi  are  divided  respiration 
becomes  much  slower,  fuller,  and  deeper  than  normal,  but  if  the  central 
end  is  stimulated  the  respiration  is  again  quickened,  and  a  strong 
stimulus  arrests  it  in  the  position  of  deep  inspiration.  Fourthly.  Affero- 
inhibitory  fibres  to  the  respiratory  centre  pass  in  tlie  superior  and  in- 
ferior laryngeal  nerves,  and  proljably,  also,  in  the  splanchnic  nerves, 
and  powerful  stimulation  of  these  fibres  produces  respiratory  arrest  in 
expiration.  Fifthly.  Efferent  fibres  connect  the  cortical  motor  centres 
with  the  respiratory  centres  in  the  medulla,  and  probably  also  directly 
with  the  spinal  centres.  Sixthly.  The  respiratory  centre  in  the  medulla 
is  connected  with  the  spinal  centres  probably  by  cells  as  well  as  by  fibres, 
and  the  former  of  these  centres  is  probably  only  the  upper  expanded 
termination  of  a  continuous  gray  column  which  forms  the  spinal  nuclei. 
Seventhly.  The  spinal  nuclei  are  connected  with  the  muscles  of  respira- 


THE    VISCERAL    KIXESIOXEU  ROSES .  211 

tion  by  the  thoracic,  phrenic,  and  spinal  accessory  nerves,  and  by  the 
nasal  branches  of  the  facial,  and  some  of  the  fibres  of  the  superior 
laryngeal  nerve.  Eighthly.  It  is  probable  that  there  is  no  localized 
sensory  cortical  centre  for  respiration,  but  the  distress  caused  by 
obstruction  to  the  breathing  is  a  complex  sensation  caused  by  irritation 
of  the  afferent  fibres  of  the  respiratory  muscles  and  various  other 
afferent  fibres. 

The  rhythmical  action  of  the  respiratory  centre  is  probably  auto- 
matic and  not  reflex  in  its  nature,  although  its  action  is  variously 
modified  by  afferent  impulses.  The  exciting  cause  of  the  respiratory 
movements  is  the  presence  of  a  certain  amount  of  oxygen  and  carbonic 
acid  in  the  blood,  respiration  becoming  stronger  the  less  the  quantity  of 
oxygen  and  the  more  of  carbonic  acid  it  holds.  The  rhythm  of  res- 
piration is,  however,  modified  and  regulated  by  impulses  passing  through 
the  afferent  inhibitory  and  accelerating  fibres.  Brener  and  Herinof 
believe  that  distention  of  the  lungs  acts  as  an  excitant  to  the  inhibitory 
fibres,  and  thus  induces  an  expiratory  act,  and  that  contraction  of  the 
lung  excites  accelerating  fibres  and  thus  initiates  an  inspiration.  It  is 
also  probable  that  we  must  assume  the  existence  of  an  inspiratory  and 
an  expiratory  centre  in  the  medulla. 

b.  Disorders  of  the  Respiratory  Nervous  Mechanism. 

(1)  Accelerated  Breathing. — When  the  blood  is  deficient  in  oxygen 
and  charged  with  carbonic  acid,  the  respiratory  centre  in  the  medulla 
is  stimulated  and  the  respiratory  rhythm  is  accelerated.  The  breathing 
is  also  often  accelerated  in  hysteria  and  other  nervous  disorders,  and 
in  febrile  diseases. 

(2)  Dyspncea. — When  respiration  is  accompanied  by  a  distressing 
consciousness  of  want  of  breath,  arising  from  undue  irritability  of  the 
nervous  mechanism,  as  in  hysteria,  or  from  insufficient  aeration  of  the 
blood,  as  in  organic  diseases  of  the  heart,  the  accessory  muscles  of  res- 
piration are  thrown  into  action,  and  the  condition  is  called  dyspnoea. 
When  there  is  an  obstruction  to  the  passage  of  air  to  and  from  the 
lungs,  the  limits  of  distention  and  contraction  are  reached  slowly  and 
Avith  effort,  and  consequently  the  dyspnoea  is  declared  not  so  much  by 
the  frequency  of  the  respiratory  movements  as  by  the  increasing  effort 
required  to  accomplish  the  act  and  by  an  alteration  in  the  ratio  of  the 
various  stages  of  the  respiratory  rhythm. 

(3)  Apnoea. — By  blowing  air  into  the  lung  or  by  forced  voluntary 
breathing  the  blood  becomes  saturated  with  oxygen  and  poor  in  car- 


k 


212  GENERAL    SYMPTOMATOLOGY. 

bonic  acid,  and  the  respiratory  movements  are  temporarily   arrested. 
This  condition  is  termed  apnoea. 

(4)  Asphyxia.— ^\\en  the  deficiency  of  oxygen  in  the  blood  is  very 
o-reat  the  excitability  of  the  respiratory  motor  centre  in  the  medulla 
becomes  destroyed,  and  the  respiratory  movements  are  arrested.  This 
condition  is  termed  asphyxia. 

(5)  Cheyne-Stokes  Respiration. — In  various  cerebral,  cardiac,  and 
renal  affections  the  breathing  becomes  intermittent.  After  a  prolonged 
pause  the  respiratory  rhythm  becomes  established,  and  the  respiration 
gradually  increases  in  depth  and  frequency  up  to  a  certain  point, 
beyond  which  they  become  gradually  shallower  and  slower  until  the 
pause,  which  may  last  from  one-half  to  three-quarters  of  a  minute. 
The  duration  of  the  whole  cycle  is  usually  from  one  to  two  m.inutes. 
This  peculiar  kind  of  breathing,  with  its  gradually  ascending  and  de- 
scending intensity  and  periodical  pause,  is  named  the  Cheyne-Stokes  res- 
piration, after  the  observers  who  first  described  it.  The  usual  explanation 
of  this  phenomenon  is  that  when  the  excitability  of  the  respiratory  centre 
is  greatly  diminished  the  blood  must  become  surcharged  with  carbonic 
acid  in  order  to  excite  it,  the  increased  inspiratory  efforts  thus  induced 
diminish  the  venous  state  of  the  blood,  and  the  respiration  becomes 
less  powerful,  until  it  is  finally  arrested  for  a  time  until  the  blood 
becomes  again  surcharged  with  carbonic  acid.  Langendorffs  experi- 
ments prove  that  arrest  of  the  flow  of  blood  to  the  medulla  will  induce 
this  kind  of  breathing  in  animals,  and  it  is,  therefore,  likely  that  an 
alteration  in  the  nutritive  quality  of  the  blood,  or  a  spasm  of  the 
arteries  of  the  medulla,  may  help  to  cause  it. 

(6)  Asthma  nervosum  consists  of  paroxysmal  attacks  of  difficulty  of 
breathing,  which  are  caused  by  a  spasmodic  contraction  of  the  muscular 
tissue  of  the  bronchial  tubes.  The  expectoration  of  frothy  mucus 
which  generally  accompanies  an  attack  would  seem  to  indicate  that  the 
symptoms  are  also  in  part  caused  by  an  oedematous  swelling  of  the 
mucous  membrane  of  the  smaller  bronchi.  Those  who  are  subject  to 
nasal  catarrh  will  readily  understand  the  suddenness  with  which  such  a 
swelling  may  appear,  and  the  degree  of  obstruction  and  discomfort  to 
which  it  may  give  rise.  The  asthmatic  paroxysm  may  be  excited  by 
direct  irritation  of  the  trunk  of  the  vagus,  in  other  cases  it  is  caused 
by  reflex  irritation  of  the  sensory  nerves  of  the  lungs  themselves,  or  of 
those  of  remote  organs,  such  as  the  stomach,  intestines,  or  uterus.  An 
attack  sometimes  results  from  central  irritation,  and  it  is  then  generally 
associated  with  hysteria.  In  some  cases  an  asthmatic  attack  is  accom- 
panied by  a  feeling  of  great  oppression  and  great  acceleration  of  the 
pulse,  which  may  beat  from  132  to  148   in  the  minute,  and  in  these 


THE    VISCEKAL    KINESIOXEUROSES.  213 

cases  it  is  probable  that  there  is  a  simultaneous  irritation  of  the  pul- 
monary and  paralysis  of  the  cardio-inhibitory  fibres  of  the  vagus. 

Sneezing,   coughing,    respiratory    spasm,   and   respiratory  paralysis 
will  be  considered  hereafter. 

4.  Disorders  of  the  Nervous  Mechanism  of  tlw  Bladder  and  Rectum. 

a.  The  Nervous  Mechanism  of  the  Bladder  and  Rectum. 
The   walls  of  the  bladder  and   rectum   contain  muscular  fibres  to 
expel  their  contents,  while  at  the  mouth  of  each  there  is  a  sphincter 
which  is  maintained  in  a  state  of  tonic  contraction,  and  thus  prevents 

Fig.  76. 


Diagram  Showing  the  Probable  Plan  of  the  Centre  for  JIictirition.  (After  Gowers.) 
5IT,  Motor  tract,  ST,  Sensory  tract  in  the  spinal  cord ;  MS,  Centre,  and  m  s,  3Iotor  nerve  for  spliincter  ; 
MD,  Centre,  and  m  d,  Motor  nerve  for  detrusor ;  s,  Afferent  nerve  from  mucous  membrane  to  S,  sensory 
portion  of  centre  ;  B,  Bladder.  At  r  the  condition  during  rest  is  indicated,  the  sphincter  centre  in  action, 
the  detrusor  centre  not  acting.  At  a  the  condition  during  action  is  indicated,  tlie  sphincter  centre 
inhibited,  the  detrusor  centre  acting. 

the  continual  escape  of  their  contents.  It  is  probable  that  the  nervous 
arrangements  for  the  regulation  of  both  the  urinary  and  rectal  func- 
tions are  the  same,  and  it  will  consequently  suffice  if  we  describe  the 
nervous  mechanism  of  the  bladder. 

This  nervous  mechanism  consists  of  nerve  centres  and  their  connec- 
tions with  one  another  and  with  the  viscus.  It  is  probable  that  two 
centres  exist  in  the  spinal  cord — an  automatic  centre  (Fig.  76,  MS) 


214  GENEEAL    SYMPTOMATOLOGY. 

situated  in  the  segments  corresponding  with  the  second,  third,  and  fourth 
sacral  nerves,  and  maintaining  the  tonic  contraction  of  the  sphincter, 
and  a  reflex  centre  (Fig.  76,  MD)  situated  on  a  little  higher  level  for 
the  expulsion  of  the  urine  by  inducing  a  contraction  of  the  detrusor 
vesicae.  Another  centre  is  situated  in  the  cortex  of  the  brain,  and  by 
its  means  the  automatic  and  reflex  lumbar  centres  are  brought  under 
voluntary  control.  The  cortical  centre  is  connected  Avith  the  lumbar 
centres  by  means  of  centrifugal  fibres  (MT),  and  the  lumbar  automatic 
and  reflex  centres  are  connected  with  the  bladder  by  eff"erent  fibres, 
some  of  which  [m  s)  connect  the  automatic  centre  (MS)  with  the 
sphincter  and  others  {m  d)  connect  the  reflex  centre  with  the  detrusor. 
These  centres  are  also  connected  with  the  periphery  by  means  of 
afierent  fibres,  some  of  them  being  reflex  and  othei'S  sensory.  The 
reflex  afierent  fibres  (s)  ascend  from  the  mucous  membrane  of  the 
bladder,  to  reach  the  lumbar  centres  through  the  posterior  gray  horns 
(S),  while  other  afi'erent  fibres  ascend  along  the  centripetal  conducting 
paths  (ST)  to  reach  the  cortex  of  the  brain,  and  then  to  become  con- 
nected with  the  cortical  centre. 

When  the  bladder  is  empty  or  only  })artially  full  the  S])hincter  is 
maintained  in  a  state  of  continuous  contraction  by  tlie  action  of  the  auto- 
matic centre  (MS).  But  when  it  becomes  distended  a  strong  impression 
is  made  upon  the  afferent  nerves  of  the  mucous  membrane  and  impulses 
are  conveyed  to  the  lumbar  centre  and  to  the  brain.  Now  the  effect  of 
afferent  impulses  upon  an  automatic  centre  is  to  inhibit  its  action,  while 
afferent  impulses  conveyed  to  a  reflex  centre  find  vent  along  eff"erent 
channels.  When,  therefore,  afferent  impulses  are  conveyed  to  the 
lumbar  centres,  the  action  of  the  automatic  centre  is  inhibited  and  the 
sphincter  relaxes,  while  that  of  the  reflex  centre  is  increased  and  the 
detrusor  vesicae  contracts.  The  action  of  the  local  automatic  and  reflex 
mechanisms  is  rendered  more  definite  and  certain  when  the  afferent 
impulses  reach  the  brain.  A  desire  to  urinate  is  excited ;  voluntary 
impulses  are  then  conveyed  by  centrifugal  cliannels  to  the  inferior  cen- 
tres, the  action  of  the  automatic  centre  is  either  increased  and  that  of 
the  reflex  centre  inhibited  so  as  to  check  tlie  reflex  tendency  to  urinate, 
or  the  action  of  the  automatic  centre  is  inhibited  and  that  of  the  reflex 
increased,  and  urination  is  accomplished. 

b.  Disorders  of  the  Vesical  ^^ekvous  Mechanism. 

The  nervous  mechanism  of  the  bladder  may  be  aff"ected  in  various 
ways,  but  those  disorders  generally  declare  themselves  either  by  incon- 
tinence or  retention.     Affections  of  the  nervous  mechanism  of   the 


I 

L 


THE    VISCERAL    KIXESIONEUROSES .  215 

bladder  may  be  divided  into  those  caused  ])y  (a)  spino-periplieral  and 
(b)  those  caused  by  cerebro-spinal  lesions. 

(a)  Spino-periphcral  Lesions. — A  destructive  lesion  of  the  automatic 
centre  of  the  sphincter,  or  of  its  efferent  fibres,  gives  rise  to  parahjtir 
or  atonic  incontinence,  while  irritative  lesions  occasion  spasmodic  reten- 
tion. A  destroying  lesion  of  the  reflex  centre  causes  paralytic  or 
atonic  retention,  and  irritative  lesions  of  the  reflex  arc,  generally 
caused  by  peripheral  irritation  of  the  afferent  fibres,  as  in  cystitis,  give 
rise  to  spasmodic  incontinence. 

(h)  Cerebrospinal  Lesions. — Destroying  lesions  of  the  cortical  cen- 
tre or  of  the  centrifugal  conducting  paths  arrest  voluntary  control  over 
the  bladder  the  urine  is  discharged  at  irregular  intervals,  and  cannot 
be  restrained  :  but  if  the  spino-peripheral  apparatus  is  free  from  disease 
the  urine  does  not  escape  in  a  continuous  stream.  If  the  centripetal 
cerebral  conducting  paths  are  also  aff'ected,  the  patient  is  unconscious 
of  the  act  of  uriiuition.  Irritative  lesions  of  the  cerebro-spinal  appa- 
ratus may  give  rise  at  one  time  to  spasmodic  incontinence,  and  at  other 
times  to  spasmodic  retention.  The  disturbances  of  the  functions  of  the 
bladder  met  with  in  cases  of  hysteria  and  during  epileptic  attacks  are 
probal)ly  caused  b}^  cerebral  discharges  along  the  cerebro-spinal  con- 
ducting paths. 

o.  Disorders  of  the  Nervous  Mechanism  of  the  Gfenital  Organs. 

a.  The  Nervous  Mechanism  of  the  Genital  Organs. 

Sexual  Functions. — The  sexual  functions  are  governed  by  a  cortical 
centre,  a  reflex  centre  situated  in  the  upper  part  of  the  lumbar  enlarge- 
ment, and  local  automatic  ganglia  connected  with  the  bloodvessels  of  the 
corpora  cavernosa.  It  is  not  necessary  to  describe  in  detail  the  connec- 
tions of  these  centres  with  one  another  and  with  the  periphery.  The 
lumbar  reflex  centre  is  stimulated  to  action  by  («)  irritation  of  the 
sensory  nerves  of  the  glans  penis,  and  (b)  discharge  from  the  cortex  of 
the  brain  with  its  associated  emotional  excitement.  On  stimulation  of 
the  reflex  centre  efferent  impulses  are  conveyed  along  the  nervi  eric/entes, 
which  cause  vascular  dilatation  and  erection  by  inhibiting  the  action  of 
the  local  automatic  ganglia.  A  still  more  prolonged  irritation  of  the 
lumbar  centre  produces  ejaculation. 

b.  Disorders  of  the  Nervous  Mechanism  of  the  Genital  Organs. 

The  sexual  functions  may  be  disordered  by  (a)  spino-peripheral,  or 
(b)  cerebro-spinal  lesions. 

(a)  Spino-peripheral  Lesions. — Destroying  lesions  of  the  lumbar 
centre  or  of  the  nervi  erigentes  cause  impotence,  while  irritative  lesions 


216  GENERAL    SYMPTOMATOLOGY. 

of  the  reflex  arc,  generally  stimulation  of  the  afferent  portion  of  the  arc, 
cause  erection  without  sexual  desire,  named  priapism,  or  partial  erec- 
tions with  strong  sexual  desire,  named  satyriasis.  In  the  latter  condi- 
tion the  cortical  centres  are  also  stimulated  either  directly  from  the 
original  source  of  irritation  or  indirectly  from  the  erections  produced. 
This  condition  is  met  with  in  cases  of  locomotor  ataxia. 

{h)  Cerebrospinal  Lesions. — Destroying  lesions  of  the  cortical  cen- 
tres or  of  the  centrifugal  conducting  paths  render  the  patient  impotent, 
but  erections  and  ejaculations  may  still  occur  so  long  as  the  reflex 
mechanism  in  the  cord  is  intact.  If  the  centripetal  paths  are  inter- 
rupted the  subject  is  insensible  of  an  erection.  The  act  of  coition  for 
instance,  affords  no  pleasure  to  many  hysterical  Avomen,  and  it  is  proba- 
ble that  in  them  there  is  a  functional  arrest  of  centripetal  impulses  to 
the  cortex  of  the  brain.  Irritati\'e  lesions  of  the  cortical  centre  or  of 
the  centrifugal  conducting  path  may  give  rise  to  satyriasis,  nympho- 
mania, or  to  priapism.  Satyriasis  in  the  male,  ov  nymphomania  in  the 
female,  are  not  unfrequently  observed  in  the  insane,  caused  probably 
by  irritation  of  the  cortex ;  and  irritation  of  centripetal  fibres  is  also 
likely  to  give  rise  to  the  same  condition.  But  although  irritation  of 
centrifugal  channels  occasions  priapism,  it  is  not  likely  to  cause  satyria- 
sis. Lesions  in  the  upper  dorsal  and  lower  cervical  regions  of  the 
cord  are  often  accompanied  by  })riapism,  doubtless  caused  by  irritation 
of  centrifugal  conducting  paths. 

6.  Disorders  of  the  Nervous  3Ii'chanisnis  of  Other  Viscera. 

It  would  occupy  too  much  space  to  enter  upon  an  analysis  of  the 
motor  affections  of  the  other  viscera,  such  as  the  various  segments  of 
the  intestines  and  the  uterus  with  its  a[)pendages.  Complicated  dis- 
orders of  these  and  other  organs  occur  from  lesions  of  the  centres  of 
innervation  in  the  cortex  of  the  brain,  medulla  oblongata,  and  spinal 
cord,  as  well  as  from  lesions  of  the  intramural  ganglia,  and  the  fibres 
which  connect  these  different  centres  with  one  another  and  the  peri- 
phery. These  lesions  give  rise  to  atony  or  hypertony,  spasm  or 
paralysis,  or  want  of  motor  coordination,  similar  in  principle  to  the 
disorders  of  the  nervous  mechanisms  we  have  just  been  considering. 

Iir.    AVASCULAR    KiNESIONEUROSES    OR    AnGIONEUROSES. 

1.    The  Vaso-motor  Nervous  Mechanism. 

The  calibre  of  the  bloodvessels  throughout  the  body  appears  to  be 
regulated  by  means  of  a  nervous  mechanism  which  is  essentially  similar 
to  those  which  regulate  the  movements  of  the  hollow  viscera.     Tlie 


THE    VASCULAR    KINESIO^'EUROSES.  217 

centres  consist  of  local  ganglia  in  the  walls  of  the  arteries,  spinal  cen- 
tres, vaso-motor  centre  in  each  lateral  half  of  the  medulla,  and  cortical 
luotor  centres  which  are  situated  in  the  motor  area  of  the  cortex.     The 
vaso-motor  centre  in  the  medulla  is  probably  only  the  upper  expanded 
end  of  a  column  of  gray  matter  which   represents   the  spinal  centres. 
The  following   are  some  of  the   conducting  fibres  of  the  vaso-motor 
mechanism  :     Firstly.  Afferent  fibres  from  the  periphery  of  the  body 
generally  alter  the  arterial   tonus.     A  medium  degree  of  irritation  of 
the  sensory  nerves  causes  an  increase,  but  strong  irritation  causes  great 
diminution  of  the  vascular  tone.     Secondly.  Afferent  fibres  which  run 
in  the  vagus,  and  which,  on  being  irritated,  cause  a  diminution  of  the 
vascular  tone,  and  these  are  consequently  named  depressor  fibres.     In 
the  rabbit  these  fibres  arise  from  the  heart,  and  form  a  separate  branch 
which  runs  alongside  the  carotid  artery  and  the  cervical  sympathetic. 
Thirdly.  Afferent  fibres  which  run  in  the  superior  laryngeal  nerve  and 
the  sympathetic,  and   excitation  of  which  causes  a  marked  increase  of 
vascular  tone,  and  conse(|uentl_y  these  fibres  are  named  pressor  fibres. 
Fourtldy.  Afferent  fibres   connect   the  muscular  fibres  of  the  middle 
coat  of  the  arteries  with  the  intramural  gano-lia,  and  excitation  of  these 
causes   first   contraction   and   then   dilatation   of  local   vascular  areas. 
Fifthly.  Centrifugal   fibres   connect   the  cortical  centres  of  one  hemi- 
sphere with  the  vaso-motor  centre  of  the  opposite  half  of  the  medulla. 
Sixthly.  Efferent  fibres   connect  the  vaso-motor  centre  in  the  medulla 
with  the  spinal  centres,  but  it  is  probable  that  the  connection  between 
these  centres  is  in  considerable  part  effected  by  means  of  gray  matter. 
Seventhly.  Efferent  fibres  connect  the  vaso-motor  fibres  in  the  medulla 
and  the  spinal  vaso-motor  centres  with  the  intramural  ganglia,  these 
fibres  passing  outwards  partly  through  the  rami  communicantes  and  the 
sympathetic,  and  partly  through  the  anterior  roots  and  the  spinal  nerves. 
These  fibres  are  of  two  kinds  :  excitation  of  one  set  of  fibres  causes 
the  arteries  to   contract,  and  these  are  consequently  named  vaso-con- 
strictor  fibres;  but  excitation  of  the  other  set  causes  the  arteries  to 
dilate,  and  these  are  consequently  named  vaso-dilator  fibres.     In  many 
parts  of  the  body  the  vaso-dilator  fibres  run  in  separate  channels  from 
the  vaso-constrictor  fibres.     Stimulation   of  the  chorda  tympani,  for 
example,,  causes   dilatation   of   the   bloodvessels   of   the   submaxillary 
glands  and  of  the  anterior  part  of  the  tongue.     In  the  extremities  the 
nerve  trunks  contain  both  kinds  of  nerve  fibres;     Eighthly.  Effei-ent 
filjres  connect  the  local  ganglia  with  the  muscular  fibres  of  the  middle 
coat  of  the  arteries. 

The  centre  in  the  medulla  oblongata  is  the  general  vaso-motor  centre 
for  all  the  arteries  of  the  body,  and  by  its  action,  which  is  probably  of 


218  GEXEEAL    SYMPTOMATOLOGY. 

a  reflex  nature,  it  maintains  all  the  arteries  of  the  body  in  a  medium 
state  of  contraction,  constituting  arterial  tonus. 

2,  Disorders  of  the  Vaso-motor  Nervous  3fechanism, 

Spasm  of  the  vessels — angiospasm  or  vascular  hypertony — may  be 
caused  by  irritation  of  vaso-constrictor  or  paralysis  of  vaso-dilator 
fibres  ;  while  dilatation  of  vessels — angioparalysis  or  vascular  atony — 
may  be  caused  by  paralysis  of  vaso-constrictor  or  irritation  of  vaso- 
dilator fibres.  Both  irritation  and  paralysis  of  vaso-motor  fibres  may 
be  direct  from  lesion  of  the  fibres  or  of  the  centres,  or  reflex  from  lesion 
of  aff"erent  fibres.  Alterations  of  the  calibre  of  the  vessels  of  the  sur- 
foce  of  the  body  may  be  caused  by  (a)  ]ieriplieral,  (/>)  spinal,  and  (/•) 
cerebral  lesions :  while  special  mention  will  be  made  {d)  of  the  vaso- 
motor disorders  of  the  viscera. 

a.  Peripheral  Ancjioneuroses 

Reflex  vascular  disorders  may  be  produced  by  lesions  of  the  afferent 
fibres  which  pass  from  the  vessels  to  the  local  ganglia,  or  of  afferent 
fibres  which  pass  to  the  ganglia  situated  higher  up.  These  reflex  dis- 
orders may  consist  of  spasm  or  dilatation,  although  it  is  not  known 
under  what  conditions  the  one  or  the  other  state  is  caused.  Dilatation 
of  the  vessels  of  the  conjunctiva,  for  example,  is  caused  by  neuralgia 
of  the  first  division  of  the  trigeminus,  but  it  is  not  known  whether  the 
action  is  reflex  or  direct,  or  whether  the  vascular  dilatation  is  caused 
by  paralysis  of  vaso-motor  constrictor  or  irritation  of  vaso-dilator  fibres. 
Division  of  large  nerve  trunks  is  followed  by  redness  and  increased 
temperature  of  the  parts  supplied  by  the  injured  nerve,  which  is  caused 
by  paralysis  of  the  vaso-constrictor  nerves.  But  degeneration  of  the 
nerve  fibres  induces  trophic  changes  in  the  affected  extremity,  which 
causes  the  material  exchanges  to  be  diminished  and  the  circulation  to 
be  less  active,  and  consequently  less  heat  is  generated,  while  more  is 
radiated  owing  to  the  dilatation  of  the  vessels,  and  the  temperature  falls 
below  the  normal.  Paralysis  of  the  vaso-motor  nerves  of  an  extremity 
occurs  sometimes  in  the  absence  of  any  other  symptom  of  nervous 
disease. 

b.  Spinal  Anoioneuroses. 

Lesions  of  the  vaso-motor  centres  in  the  medulla  and  spinal  cord,  or 
of  their  respective  conducting  paths,  may  increase  or  diminish  the 
arterial  tone  either  locally  or  generally.  Injuries  and  diseases  of  the 
spmal  cord  which   cause  paraplegia  are  generally  associated  by  a  pri- 


THE    VASCULAR    KINESIONEUROSES.  219 

maiy  increase  of  temperature  of  the  paralyzed  limbs.  In  hemipara- 
plegia  of  spinal  origin  there  is  a  primary  increase  of  temperature  in 
the  paralyzed  as  compared  with  the  non-paralyzed  limb. 

Injuries  of  the  cervical  portion  of  the  cord  near  the  medulla  oblon- 
gata cause  a  remarkable  elevation  of  the  temperature  of  the  body,  and 
in  these  cases  the  temperature  may  continue  to  rise  after  the  injurv. 
and  may  even  increase  considerably  after  death.  This  remarkable  rise 
of  temperature  probably  depends  upon  sudden  paralysis  of  the  vaso- 
motor system,  or  upon  interference  with  the  action  of  a  heat-regulating 
centre  in  the  medulla  oblongata.  In  locomotor  ataxia,  again,  which  is 
a  disease  of  the  afferent  or  sensory  portion  of  the  spinal  cord,  the  lower 
extremities  are  often  cold  from  vascular  spasm,  and  in  some  cases  of 
this  disease  a  local  alteration  of  the  vessels  occurs  Avhich  is  so  remark- 
able as  to  require  special  mention. 

Tabetic  JEcchi/Dioscs. — In  the  course  of  locomotor  ataxia,  patches  of 
discolored  skin  are  found  scattered  irregularly  over  the  lower  extremi- 
ties and  lower  part  of  the  trunk.  These  patches  are  at  first  of  a  bright 
red  color,  but  soon  become  purple,  and  pass,  like  ordinary  ecchymoses, 
through  various  shades  of  brown,  green,  and  yellow,  until  they  finally 
fade  from  the  circumference  to  the  centre,  and  disappear  in  from  four  to 
six  days  from  the  commencement.  These  ecchymoses  appear  suddenly 
towards  the  termination  of  severe  paroxysms  of  lancinating  pains  and 
gastric  crises.  They  are  irregularly  circular  in  form,  and  vary  in  size 
from  a  few  lines  to  more  than  an  inch  in  diameter.  Several  of  these 
patches  are  found  at  the  same  time,  as  many  as  three  or  four  of  them 
being  observed  on  each  lower  extremity. 

The  local  asphyxia  of  Renaud  belongs  probably  to  the  angioneuroses, 
but,  as  it  often  terminates  in  gangrene,  its  description  will  be  found 
amongst  the  trophoneuroses. 

c.  Cerebral  Angioneuroses. 

Vaso-motor  disorders  are  daily  observed  under  the  influence  of 
various  emotions,  the  most  familiar  of  these  being  the  blush  of  shame 
and  the  pallor  of  fear.  Fainting  is  associated  with  pallor  of  the  sur- 
face, and  alternatincr  conditions  of  pallor  and  redness  are  often  observed 
in  various  neuroses,  such  as  hysteria  and  epilepsy.  At  other  times  the 
vascular  alteration,  instead  of  being  diffused,  occurs  in  patches — what 
has  been  observed  under  the  name  of  cerebral  maculae. 

Taches  cerebrales  consist  of  red  blotches  and  mottlings  on  the  chest 
or  abdomen  of  epileptics,  and  those  suffering  from  Graves's  disease  and 
other  neuroses.  When  the  affected  portion  of  skin  is  rubbed,  or,  ni 
strongly  marked  cases,  is  merely  touched  by  the  finger,  the  surface  soon 


220  GENERAL    SYMPTOMATOLOGY. 

becomes  suffused  ^vitll  bright  red  marks,  which  spread  to  some  distance 
around  the  point  touched,  and  persist  for  several  minutes. 

d.  Visceral  Axgioneuroses. 

The  vaso-motor  nerves  of  the  thoracic  viscera  are  derived  from  the 
inferior  cervical  and  superior  tlioracic  ganglia,  and  from  the  spinal 
cord  bv  communicating  branches  from  the  third  to  the  seventh  dorsal 
vertebrge.  The  vaso-motor  nerves  of  the  abdominal  viscera  exist 
chiefly  in  the  splanchnic  nerves.  Section  of  the  splanchnic  nerves 
occasions  a  great  diminution  of  the  arterial  pressure  from  dilatation  of 
the  vessels  and  engorgement  of  the  abdominal  viscera.  Irritation  of 
the  distal  end  causes  contraction  of  the  vessels  and  conseciuent  eleva- 
tion of  the  blood  pressure.  A  part  of  the  vaso-motor  nerves  of  the 
abdominal  viscera  probably  passes  in  the  vagus.  Experimental  in- 
jury of  the  lumbar  portion  of  the  spinal  cord  in  animals  has  been 
found  to  cause  congestion  and  even  extravasation  of  blood  in  the 
suprarenal  capsules,  and  hemorrhagic  foci  have  been  found  in  these 
organs  in  cases  of  acute  myelitis.  Crushing  of  the  pons  and  basal 
ganglia  in  animals  has  l^een  found  to  cause  congestion  and  ecchy- 
moses  in  the  lungs,  pleura,  kidneys,  and  nmcous  membrane  of  the 
stomach  and  bowels,  and  Eulenburg  found  intestinal  hemorrhage  after 
bruising  the  cortex  of  the  occipital  lobe  of  the  brain.  Congestion 
and  extravasations  of  blood  in  the  internal  organs  are  not  uncom- 
mon as  complications  of  cerebral  apoplexy.  The  various  menstrual 
disorders  which  are  so  frequently  associated  with  emotional  disturb- 
ances are  no  doubt  the  result  <)f  functional  disorders  of  the  vaso-motor 
nerves,  and  the  vicarious  hemorrhages  of  the  stomach,  intestines,  lungs, 
and  other  organs  probably  also  depend  iijjon  disorder  of  vaso-motor 
innervation.  Both  quantitative  and  (pialitative  anomalies  in  the  con- 
dition of  the  urine  probably  de])end  upon  disorder  of  the  vaso-motor 
nerves  of  the  kidneys.  Bernard  found  that  injury  of  the  upper  part 
of  the  floor  of  the  fourth  ventricle  causes  polyuria  and  albuminuria, 
while  injury  of  the  lower  part  of  the  floor  of  the  fourth  ventricle 
causes  temporary  glycosuria.  Injuries  of  the  spinal  cord,  in  the  cervi- 
cal and  thoracic  ganglia,  or  of  the  large  nerve-trunks,  such  as  the 
sciatic  nerve,  are  also  followed  by  glycosuria.  If  the  pneumogastric 
nerve  is  divided  in  the  neck,  stimulation  of  the  upper  end  is  followed 
by  dilatation  of  the  vessels  of  the  liver,  and  the  appearance  of  sugar 
in  the  urine.  The  most  reasonable  explanation  of  these  phenomena  is 
that  vaso-motor  paralysis  of  the  hepatic  artery  causes  engorgement  of 
the  hepatic  vessels,   which   gives  rise  to  an   increased   production   of 


THE    VASCULAR    KUSTESIONEUROSES.  221 

sugjir.  Certain  forms  of  enlargement  of  the  liver  and  spleen  are 
l^robably  caused  by  paralysis  of  vaso-motor  nerves.  Section  of  tlie 
cfterent  fi))res  of  the  semilunar  and  splenic  plexuses  in  animals  causes 
enlargement  of  the  spleen,  while  ii-ritation  of  these  fibres  reduces  its 
size  and  renders  the  organ  paler.  Extirpation  of  the  coeliac  and 
mesenteric  plexuses  causes,  besides  other  phenomena,  congestion  and 
enlargement  of  the  liver,  and  it  is  probable  that  the  congestion  of  this 
organ  which  takes  place  during  attacks  of  migraine  is  of  vaso-motor 
oriirin. 


CHAPTEK  YIII. 

GENERAL  TREATMENT. 

Nervous  diseases  must  be  treated  according  to  the  same  general 
principles  as  all  other  diseases,  and  it  is  therefore  unnecessary  to  entei- 
upon  a  detailed  description  of  treatment  in  this  place.  The  treatment 
of  nervous  diseases  may  be  divided  into  that  which  is  directed :  (1)  to 
prevent  disease ;  (2)  to  remove  the  exciting  cause  of  the  disease ;  (3) 
to  remove  the  anatomical  cause ;  and  (4)  to  allay  or  remove  serious 
symptoms. 

1.  PROPHYLACTIC   TREATMENT. 

Prophylactic  treatment  consists  of  a  special  application  of  hygienic 
rules  to  the  cases  of  those  who  manifest  inherited  or  acquired  proclivi- 
ties to  diseases  of  the  nervous  system.     The  children  of  parents  who 
have  suffered  from  severe  nervous  diseases,  like  hysteria,  epilepsy,  or 
neuralgia,  ought  to  be  specially  guarded   against  being   subjected   to 
severe  mental  strain  and  emotional  excitement  in  youth,  and  especially 
during  the  period  of  sexual  development.    The  children  of  such  parents 
are  generally  quick  in  their  perceptive  ficulties  and  are  possessed  even 
of  great  intellectual  activity,  and  they  ought  not  to  be  allowed  to  enter 
upon  competitive  examinations   at   schools  except  under  the  strictest 
precautions.    Parents  and  teachers  ought  to  pay  great  attention  to  such 
symptoms  as  headache,  sleeplessness,  horrible  dreams  and  night  starl- 
ings, and  loss  of  flesh  and  appetite,  Avhich  are  the  more  usual  symptoms 
of  an  overstrained  nervous  system.     Of  these  symptoms,  sleeplessness 
is  probably  the  most  important  as  a  danger  signal,  inasmuch  as,  on  the 
one  hand,  it  is  generally  caused,  especially  in  the  absence  of  pain,  by 
exhaustion  of  the  nervous  system,  and,  on  the  other  hand,  it  becomes  a 
powerful  cause  of  further  exhaustion,  because  the  nervous  energies  used 
up  during  the  day  fail  to  be  restored  at  night.     Plenty  of  muscular 
exercise,  so  long  as  it  is  thoroughly  enjoyed  and  stops  short  of  inducing 
fatigue,  is  the  most  powerful  means  we  possess  of  fortifying  the  nervous 
system  in  young  people.    Those  who  inherit  a  predisposition  to  nervous 
disease  also  require  an  abundance  of  plain  and  nourishing  diet,  and  a 
due  exposure  to  sunlight  and  fresh  air. 


REMOVAL    OF    THE    ANATOMICAL    CAUSE.  228 

2.  REMOVAL  OF  THE  EXCITING  CAUSE. 

When  a  disease  of  the  nervous  system  has  been  induced  by  unfavor- 
able circumstances  of  climate,  exposure  to  variations  of  temperature, 
or  excessive  fatigue,  these  conditions  must,  if  possible,  be  corrected  • 
and  Avhen  the  disease  has  been  caused  by  wounds,  contusions,  or  com- 
pression of  nervous  tissues,  these  causes  must  be  removed,  and  the 
damage  done  to  the  tissues  repaired  as  much  as  possible  by  suro-ical 
interference.  If  the  disease  is  caused  by  a  morbid  poison  like  syphilis, 
malaria,  gout,  rheumatism,  or  the  metallic  poisons,  the  treatment  must 
be  directed  to  remove  these  poisons  from  the  system  or  to  neutralize 
their  action. 

3.  REMOVAL  OF  THE  ANATOMICAL  CAUSE. 

The  nutrition  of  diseased  nervous  tissues  may  be  favorably  influenced 
by  agents  which  act  directly  on  the  nervous  tissues  themselves,  the 
connective  tissues  which  surround  the  nervous  tissues,  the  vaso-motor 
nerves  and  centres  of  the  bloodvessels  themselves,  and  the  blood.  The 
agents  by  which  nutrition  can  be  influenced  may  be  divided  into  (a) 
internal  and  [b)  external  remedies. 

(a)  Internal  Remedies. 

Internal  remedies  produce  their  action  after  gaining  admission  into 
the  circulation  either  by  being  absorbed  through  the  mucous  membranes, 
skin,  or  subcutaneous  tissues  after  injection,  or  by  direct  injection  into 
a  vein.  The  following  are  some  of  the  remedies  of  this  class  :  Strychnia 
and  the  preparations  of  nux  vomica  increase  the  irritability  of  the  gray 
substance  of  the  sj^inal  cord  and  diminish  its  specific  resistance,  and 
they  are  usefully  administered  when  the  irritability  is  depressed. 
Strychnia  is  a  powerful  remedy  in  atonic  dyspepsia,  constipation  with 
flatulence,  paralysis  of  the  sphincters,  nocturnal  incontinence  of  urine, 
and  sexual  debility ;  but  does  not  possess  much  value  in  the  treatment 
of  organic  diseases  of  the  spinal  cord,  being  valueless  in  chronic  spinal 
affections  and  positively  injurious  in  all  acute  organic  aff'ections. 
Conium  depresses  the  irritability  of  the  spinal  cord  and  of  the  motor 
nerves,  and  its  use  has  been  recommended  by  Dr.  Crichton  Browne  in 
acute  mania,  and  it  has  likewise  been  found  useful  in  tetanus.  CaJahar 
bean  lessens  and  ultimately  destroys  the  irritability  of  the  gray  sub- 
stance of  the  spinal  cord,  causing  anaesthesia,  loss  of  reflex  excitability, 
and  paralysis.     It  has  been  found  useful  in  tetanus  and  in  hemicrania. 


224.  GENERAL    TEEATMENT. 

Its  alkaloid,  physostig)>ia,  iucreases  the  irritability  of  the  terminal  fibres 
of  the  vagus,  and  kills  by  paralyzing  the  respiration.  Belladonna  and 
its  alkaloTd,  atrojnne,  increase  the  irritability  of  the  gray  substance  of 
the  spinal  cord,  and  stimulate  in  a  special  manner  the  respiratory  and 
vaso-motor  centres,  the  cardiac  acceleratory  nerve  or  its  centre,  and  the 
pupillary  fibres  of  the  sympathetic  to  the  eyes.  It  paralyzes  the  motor 
nerves,  first  aifecting  those  of  the  trunk,  the  terminations  of  the  vagi 
both  in  the  heart  and  lungs,  the  terminations  of  the  secretory  nerves  of 
the  salivary  glands  and  of  the  sweat  glands,  the  terminations  of  the 
inhibitorv  fibres  of  the  splanchnics,  and  the  terminations  of  the  nerves 
supplying  the  iris.  In  large  doses  it  depi-esses  the  functions  of  the 
afferent  nerves.  This  drug  has  been  found  useful  in  cliecking  profuse 
sweating,  especially  the  night  sweats  of  phthisis,  and  the  secretion  of 
milk.  It  is  also  useful  in  habitual  constipation,  Avhooping  cough, 
incontinence  of  urine,  and  nocturnal  emissions;  and  its  use  has  been 
recommended  bv  Brown-Sequard  in  chronic  organic  spinal  diseases  on 
the  grounds  that  it  contracts  the  arterioles  of  the  cord.  It  is  also 
useful  in  allaying  pain,  but  is  inferior  to  opium.  JEr(/ot  is  given  in 
chronic  spinal  affections,  being  supposed  to  have  the  power  of  contract- 
intr  the  arterioles.  Opium  lessens  the  irritability  of  the  sensory  con- 
ducting paths  and  of  the  perceptive  centres.  Small  doses  first  increase 
the  irritability,  but  the  primary  increase  is  soon  followed  by  a  secondary 
stage  of  depression,  and  if  a  large  dose  be  administered  the  first  stage 
of  increased  irritability  is  so  transitory  that  it  may  be  overlooked. 
Opium  may  be  administered  in  small  doses  so  as  to  obtain  tlie  primary 
or  stimulant  action,  and  given  in  this  way  it  is  foun<l  useful  in  the 
treatment  of  nervous  exhaustion  caused  by  mental  anxiety  and  over- 
work. It  is,  however,  most  frequently  given  in  large  doses,  and  is  the 
most  powerful  remedy  we  possess  for  allaying  pain  and  procuring  sleep. 
Hydrate  of  chloral  in  small  do^es  induces  sleep,  and  in  large  doses 
profound  coma.  It  paralyzes  sensation  and  reflex  action  and  causes 
arrest  of  respiration,  or  paralyzes  the  heart.  Chloral  and  allied  agents 
are  given  in  relatively  large  doses  with  the  view  of  depressing  the 
irritability  of  the  sensory  mechanism  and  ])rocuring  sleep.  Chloral 
has  been  found  useful  in  the  treatment  of  tetanus  and  of  poisoning  by 
strychnia,  and  as  a  sedative  and  hypnotic  in  cases  in  which  the  irrita- 
bility of  the  nervous  mechanism  is  increased.  Bromide  of  potassiimi 
and  its  allies  depress  the  irritability  of  the  gray  matter  of  the  brain 
and  spinal  cord,  and  in  large  doses  diminish  sensibility  and  reflex 
excitability.  They  are  very  valuable  remedies  in  epilepsy  and  various 
other  spasmodic  affections.  Preparations  of  zi7ic,  arsenic,  and  phos- 
2)horus  appear  to  exercise  a  fovorable  influence  on  the  nutrition  of  the 


REMOVAL    OF    THE    ANATOMICAL    CAUSE.  225 

nervous  system,  and  they  have  consequently  been  named  "  nervine 
tonics."'  These  agents  have  been  found  useful  in  cases  of  neurasthenia, 
ejiilepsy,  chorea,  liysteria,  and  various  spasmodic  affections.  Silver 
salts  also  belong  to  the  same  class  of  agents,  and  they  have  been 
employed  in  the  treatment  of  epilepsy  and  tabes  dorsalis.  Iron,  bv 
imjjroving  the  quality  of  the  l)lood,  is  a  most  useful  remedy  in  various 
nervous  affections,  and  large  doses  of  the  carbonate  are  particularly 
efficacious  in  neuralgic  affections.  Quiniyie  is  a  specific  against  all 
nervous  affections  which  result  from  malaria,  but  it  is  also  useful  in  the 
treatment  of  neuralgia,  and  especially  in  neuralgia  of  the  supra-orbital 
branch  of  the  fifth  nerve.  Milk,  whey,  and  grape  '■^  cures,"  and 
courses  of  mineral  ivaters,  act  beneficially  in  many  nervous  diseases  by 
exercising  a  favorable  influence  on  general  nutrition.  Iodide  of  potas- 
sium has  probably  no  special  action  on  the  nervous  tissues  themselves, 
but  its  well-known  action  in  quickening  the  absorption  of  inflammatory 
effusions  renders  it  an  invaluable  agent  in  the  management  of  many 
nervous  diseases,  and  it  is  an  indispensable  agent  in  the  treatment  of 
syj)hilitic  nervous  diseases.  Mercurial  preparations  are  also  useful  in 
tlie  treatment  of  inflammatory  diseases,  more  especially  when  the  mem- 
branes of  the  brain  or  spinal  cord  or  the  sheaths  of  nerves  are  affected. 
Mercurial  treatment  is,  however,  chiefly  directed  against  syphilitic 
nervous  diseases. 

(b)  External  Remedies. 

Cold  steadily  applied  lowers  the  irritability  and  retards  the  conduc- 
tivity of  the  nervous  tissues,  and  consequently  it  is  used  as  a  remedy 
in  the  acute  stage  of  all  inflammatory  affections  of  the  nervous  system. 
Chapman's  vaso-motor  therapeutics  is  founded  on  the  assumption  that 
cold  applied  to  the  spine  lowers  the  irritability  of  the  vaso-motor,  along 
with  the  other  centres  of  the  spinal  cord,  and  thus  causes  dilatation  of 
the  bloodvessels  whose  nervous  supply  is  derived  from  the  portion  of 
the  cord  over  which  the  cold  is  applied.  Chapman's  ice-bag  is  the  best 
method  of  applying  cold  to  the  spine,  and  very  convenient  bags  are 
made  for  applying  ice  to  the  head  or  any  other  part  of  the  body. 

Warmth  increases  the  irritability  and  accelerates  the  conductivity  of 
the  nervous  tissues,  and  when  combined  with  moisture  it  relaxes  the 
tissues,  and  thus  exercises  a  soothing  influence  in  painful  and  spasmodic 
affections.  Warmth  may  be  applied  by  means  of  hot-water  fomenta- 
tions, poultices,  Priessnitz's  compresses,  hot  sand-bags,  and  India-rubber 
bags  filled  with  liot  water. 

Cold  baths  tend  directly  to  lower  the  irritability  of  the  nervous   tis- 

15 


226  GENERAL    TREATMENT. 

sues  and  to  depress  the  nervous  functions,  and,  when  their  use  is  attended 
with  benefit,  it  is  due  to  their  indirect  action,  or  to  the  reaction  of  the 
tissues.  This  reaction  is  aided  by  the  presence  of  salt  in  the  water, 
and  consequently  the  sea  bath  is  less  depressing  than  the  ordinary  bath. 
The  cold  bath  is  a  powerful  therapeutic  agent  in  neurasthenia,  hysteria, 
and  various  other  functional  afiections,  and  it  may  occasionally  be  found 
useful  in  chronic  organic  aflFections.  SJiowcr,  douche,  and  sponge  baths 
produce  powerful  nervous  stimulation  by  the  impact  of  Avater  on  the 
body,  in  addition  to  the  effects  of  the  cold  immersion.  Shower  and 
sponge  baths  are  useful  in  the  treatment  of  functional  nervous  affec- 
tions ;  while  the  douche  is  employed  for  its  local  effects  on  paralyzed 
parts,  and  in  rousing  a  patient  from  drunkenness  or  opium  poisoning. 
TFarm  baths  act  as  a  sedative  to  the  cutaneous  nerves,  and  through 
them  to  the  nervous  system  generally. 

If  the  temperature  be  indifferent  (90°  to  97°  F.)  the  bath  acts 
mainly  as  a  nervous  sedative,  while  warm  and  hot  baths  (97°  to  108°  F.) 
produce  great  vascular  excitement  and  act  as  powerful  nervous  stimu- 
lants. If  the  symptoms  of  irritation  preponderate  the  indifferent  baths 
should  be  selected,  and  if  the  symptoms  of  depression  are  prominent 
the  warm  and  hot  baths  are  to  be  preferred.  Brine,  vapor,  hot-sand, 
hot-air,  gaseous,  and  chalybeate  baths  all  act  on  the  same  ])rinci])le  as 
hot  baths,  and  are  to  be  used  when  powerful  stimulation  is  required. 
The  needle  bath  is  also  a  powerful  stimulant  and  is  used  when  the 
symptoms  of  depression  predominate. 

Mud  baths  act  like  warm  baths,  but  are  much  less  exciting  than 
warm-water  spring  baths,  and  they  are  consequently  adapted  for  the 
treatment  of  spinal  irritation  and  of  the  various  forms  of  spasmodic 
paralysis. 

The  Turkish  bath  combines  many  of  the  properties  of  the  hot  and 
cold  bath.  The  great  heat  to  which  the  body  is  subjected  tends  doubt- 
less to  induce  debility,  but  the  subsequent  free  application  of  cold 
water  excites  the  cutaneous  nerves  and  braces  the  system,  so  that  the 
tonic  effects  of  the  cold  bath  are  secured.  The  systematic  kneading  to 
which  all  the  muscles  of  the  body  are  subjected  promotes  their  own 
nutrition  and  that  of  the  nerves  which  supply  them,  and  thus  the 
effects  of  the  bath  are  combined  with  those  which  result  from  careful 
and  regulated  exercise,  and  systematic  gymnastics.  The  Turkish  bath 
is,  indeed,  a  powerful  therapeutic  agent,  and  has  a  wide  range  of  use- 
fulness in  the  treatment  of  various  nervous  affections. 

Experience  has  shown  that  certain  climates  and  regions  exercise  a 
favorable  influence  on  various  nervous  diseases,  especially  on  those  of 
functional  origin.     Sea  air  has  a  very  invigorating  effect  on  the  system, 


REMOVAL    OF    THE    ANATOMICAL    CAUSE.  227 

and  it  is  well  adapte<I  for  the  cure  of  nervous  exhaustion  from  overwork 
in  those  who  are  otherwise  strong  and  healthy,  Feehle  and  irritable 
people,  however,  obtain  greater  benefit  from  residence  in  a  mountainous 
district.  Mountain  exercise  has  a  very  enlivening  effect  upon  the  ner- 
vous system,  and  the  higher  and  drier  the  district  the  more  marked  are 
the  tonic  effects.  The  Engadine  and  Davos  Platz  are  favorite  moun- 
tain residences,  and  the  Scottish  mountains,  the  English  lake  district, 
and  Ilkley,  in  Yorkshire,  are  also  favorite  places  of  resort,  although 
they  have  neither  the  elevation  nor  the  dry  atmosphere  of  the  Swiss 
mountains. 

Bhodletting  ayid  counter-irritation  are  as  useful  in  the  treatment  of 
inflammatory  affections  of  the  nervous  system  as  in  those  of  other 
organs,  but  as  they  present  nothing  special  in  their  action  or  mode  of 
application  when  employed  in  the  treatment  of  nervous  diseases,  they 
do  not  require  further  consideration  at  present.  The  counter-irritants 
usually  employed  are  cutaneous  faradization,  sinapisms,  vesicants, 
issues,  moxge,  and  the  actual  cautery.  External  frictions  are  carefully 
employed  in  various  nervous  affections.  Frictions  with  soothino-  lini- 
ments, warm  oil,  and  ointments  containing  opium  or  belladonna,  are 
used  to  allay  pain  in  neuralgic  and  other  painful  affections.  Frictions 
with  spirituous  liniments,  either  alone  or  combined  with  other  stimu- 
lants, such  as  ammonia  and  camphor,  are  used  in  the  treatment  of 
various  forms  of  paralysis. 

Seclusion  of  patients  from  their  friends  is  of  great  value  in  the 
treatment,  not  only  of  the  graver  psychoses,  but  also  of  many  cases  of 
hysteria,  neurasthenia,  melancholia,  and  other  functional  affections. 
With  reference  to  the  treatment  of  neurasthenia.  Dr.  S.  Weir  Mitchell 
says:  "Once  separate  the  patient  from  the  moral  and  physical  sur- 
roundings which  have  become  part  of  her  life  of  sickness,  and  you  will 
have  made  a  change  which  will  be  in  itself  beneficial,  and  will  enor- 
mously aid  in  the  treatment  which  is  to  follow."  One  of  the  most 
frequent  questions  which  the  physician  has  to  decide  in  the  treatment 
of  nervous  diseases  is  whether  a  patient  is  to  take  exercise  or  rest. 
This  question  is  readily  decided  in  most  cases  of  organic  disease,  the 
general  rule  being  that  physiological  rest  should  be  enjoined  in  all 
acute,  and  a  certain  amount  of  graduated  exercise  in  chronic  affections. 
In  the  minor  deg-rees  of  neurasthenia  and  melancholia  a  moderate  de- 
gree  of  exercise  may  be  prescribed,  but  it  should  be  always  short  of 
fatigue,  and  in  aggravated  cases  the  most  absolute  rest  should  be 
enjoined,  while  the  place  of  exercise  is  to  some  extent  supplied  by 
massage. 

Massage  is  a  general  term  which  includes  methodical  rubbing,  strok- 


228  GENEKAL    TKEATMEJSTT. 

ing,  kneading,  and  clapping  the  surface  of  feeble  and  paralyzed  parts— 
a  "method  which  is  often  successful  in  the  treatment  of  organic  and 
functional  paralyses.  Massage  has  been  extensively  used  in  the  Man- 
chester Royal  Infirmary  by  my  colleague,  Dr.  Morgan,  and  with  very 
gratifying  results.  The  directions  for  carrying  out  the  process  as 
practised  by  Dr.  Morgan  are  briefly  the  following : 

1.  Pinch  the  surfiice  of  the  skin  from  below  upwards,  with  the  view 
of  stimulating  the  cutaneous  nerves.  Suppose  the  lower  extremities  to 
be  paralyzed,  the  skin  of  the  foot  is  first  drawn  up  into  successive  folds 
and  lioh'tly  pinched.  The  skin  over  the  Avhole  of  the  leg,  and  finally 
that  of  the  thigh  is  gone  over  in  the  same  way. 

2.  Give  passive  movements  to  the  joints,  first  moving  each  of  them 
separately  and  then  all  together. 

3.  Shampoo  the  limb  well.  This  is  done  by  lubricating  it  with  some 
bland  oil,  which  is  well  rubbed  into  the  surface  by  the  tips  of  the 
fino-ers  passing  from  l)elow  upwards,  the  spaces  between  the  muscular 
groups  being  specially  selected  for  rubbing. 

4.  Work  the  muscles  well  with  the  fingers.  Each  muscle,  or  group 
of  muscles,  is  grasped  between  the  ball  of  the  thuml)  and  the  fingers, 
and  well  kneaded  and  rolled.  During  this  process  the  limb  nnist  be 
placed  in  a  position  to  appi'oximate  the  ends  of  the  muscles  operated 
upon,  and  thus  relax  them  to  the  utmost. 

5.  Slap  the  muscles  well  with  the  ulnar  border  of  the  hand. 

6.  Grasp  the  lower  portion  of  the  limb  between  the  hands,  and  then 
draw  them  slowly  and  firmly  upwards.  This  movement  should  be 
repeated  some  twelve  or  fifteen  times.  In  this  manner  the  veins  are 
emptied  and  the  circulation  quickened. 

The  IFciV  Mitchell  treatment.,  which  has  been  carried  out  so  success- 
fully l)y  Dr.  Playfair,  of  London,  in  the  treatment  of  neurasthenia,  is 
a  combination  of  seclusion,  rest,  massage,  and  hyperfeeding.  With 
regard  to  the  carrying  out  of  this  treatment  Dr.  Playfair  remarks : 
"  The  removal  of  the  patient  from  her  home  surroundings,  and  lier 
complete  isolation  in  lodgings  with  only  a  nurse  in  attendance,  is  a 
matter  of  paramount  importance.  This  is  a  point  on  which  I  am  most 
anxious  to  lay  stress,  since  it  is  the  great  crisis  to  the  patient  and  her 
friends,  and  constant  appeals  are  made  to  modify  this,  which  I  look 
upon  as  an  absolute  sine  qua  non.  I  attribute  much  of  the  success 
which  I  have  been  fortunate  enough  to  obtain  in  my  cases,  to  a  rigid  ad- 
herence to  this  rule."  Great  care  must  be  exercised  in  the  selection  of 
a  suitable  nurse,  and  if  the  case  is  not  going  on  favorably  much  advan- 
tage is  often  obtained  by  a  change  of  nurse.  The  patient  is  ordered  to 
bed  for  from  six  weeks  to  two  months,  and  during  the  greater  part  of 


REMOVAL    OF    THE    ANATOMICAL    CAUSE.  229 

this  period  such  actions  as  sewing,  reading,  and  writing  are  strictly- 
forbidden.  In  aggravated  cases  the  patient  is  not  allowed  even  to  turn 
over  in  bed  without  aid.  She  is  fed  by  the  nurse,  and  even  the  calls 
of  nature  are  obeyed  in  the  recumbent  posture.  With  regard  to  the 
use  of  massage  and  feeding,  Dr.  Playfair  says:  "Massage  consists  in  a 
systematic  and  thorough  kneading  and  movement  of  the  whole  muscu- 
lar system  for  about  three  hours  daily,  the  result  of  which  at  first  is  to 
produce  great  fatigue,  and  subsequently  a  pleasant  sense  of  lassitude. 
Subsidiary  to  this  is  the  use  of  the  faradic  current  for  about  ten  to 
twenty  minutes,  twice  daily,  by  which  all  the  muscles  are  thrown  into 
strong  contraction,  and  the  cutaneous  circulation  is  rendered  excessively 
active.  The  two  combined  produce  a  large  amount  of  muscular  waste, 
which  is  supplied  by  excessive  feeding,  and  in  consequence  of  the  in- 
creased assimilation  and  improved  nutrition  we  have  the  enormous  gain 
in  weight  and  size  which  one  sees  in  these  cases,  it  being  quite  a 
common  thing  for  a  patient  to  put  on  from  one  to  two  stones  in  weight 
in  the  course  of  five  to  six  weeks.  The  feeding  at  regular  intervals 
constitutes  a  large  part  of  the  nurse's  work.  At  first  from  three  to 
five  ounces  of  milk  are  given  every  few  hours,  and  the  first  few  days 
the  patient  is  kept  on  an  exclusively  milk  diet.  By  this  means  dys- 
peptic symptoms  are  relieved,  and  the  patient  is  prepared  for  the 
assimilation  of  other  food.  This  is  added  by  degrees,  pari  passu  with 
the  production  of  muscular  waste  by  massage,  which  is  commenced  on 
the  third  or  fourth  day.  By  about  the  tenth  day  the  patient  is  sham- 
pooed for  an  hour  and  a  half  twice  daily,  and  by  this  time  she  is  able 
to  take  an  amount  of  food  that  would  appear  almost  preposterous  did 
not  one  find  by  experience  how  perfectly  it  is  assimilated  and  how 
rapidly  flesh  is  put  on.  It  is  the  usual  thing  for  patients  to  take,  when 
full  diet  is  reached,  in  addition  to  two  quarts  of  milk  daily,  three  full 
meals,  viz.,  breakfast,  consisting  of  a  plate  of  porridge  and  cream,  fish 
or  bacon,  toast  and  tea,  coffee  and  cocoa;  a  luncheon,  at  1  p.m.,  of 
fish,  cutlets  or  joints,  and  a  sweet,  such  as  stewed  fruit  and  cream,  or  a 
milky  pudding;  dinner  at  7  p.m.,  consisting  of  soup,  fish,  joints,  and 
sweets,  and  in  addition  a  cup  of  raw  meat  soup  at  7  a.  m.  and  11  p.  m. 
It  is  really  very  rare  to  find  the  slightest  inconvenience  from  this  enor- 
mous dietary.  Should  there  be  an  occasional  attack  of  dyspepsia,  it  is 
at  once  relieved  by  keeping  the  patient  for  four  and  twenty  hours  on 
milk  alone." 

The  results  obtained  by  means  of  this  treatment  have  been  so  striking 
and  remarkable  that  not  the  slightest  detail  in  the  method  of  carrying 
it  out  is  unimportant.  After  the  first  few  days  of  treatment  a  consider- 
able quantity  of  soup  made  from  raw  beef  is  added  to  the  milk  diet. 


230  GENERAL    TREATMENT. 

The  following  is  Dr.  Mitchell's  formula  for  this  soup :  "  Take  one 
pound  of  raw  fillet  of  beef,  chop  it  finely,  and  place  it  in  a  bottle  with 
a  i)int  of  water  and  five  drops  of  hydrochloric  acid.  Stand  the  mixture 
in  ice  all  night,  and  in  the  morning  set  the  bottle  in  a  pan  of  water  at 
110°  F.,  and  keep  it  two  hours  at  this  temperature.  It  is  then  to  l^e 
thrown  on  a  stout  cloth,  and  strained  until  the  remaining  mass  is  nearly 
dry.  The  filtrate  is  given  in  two  or  three  doses  in  the  course  of  twenty- 
four  hours.  If  the  raw  taste  prove  very  objectionable,  the  beef  to  be 
used  may  be  quickly  roasted  on  one  side,  and  then  the  process  is  com- 
pleted in  the  manner  above  described.  The  soup  thus  made  is  for  the 
most  part  raw,  but  has  also  the  flavor  of  cooked  meat." 

Swedish  gymnastws  are  a  mere  modification  of  ordinary  gymnastics, 
the  object  being  to  aid  the  recovery  of  paralyzed  or  rather  paretic  parts 
bv  bringing  the  muscles  into  methodical  exercise.  The  patient  is 
instructed  to  make  systematic  voluntary  efforts  to  move  the  paralyzed 
muscles,  and  when  a  certain  degree  of  voluntary  movement  is  attained 
the  effect  is  increased  by  the  opposition  of  a  practised  assistant.  If, 
for  example,  the  flexors  of  the  forearm  are  to  be  exercised,  the  forearm 
is  first  extended,  and  the  patient  endeavors  to  flex  it  "whilst  the  assistant 
opposes  flexion  with  more  or  less  force.  In  the  case  of  associated 
movements  it  is  often  necessary  to  aid  the  contraction  of  one  grouj)  of 
muscles  so  as  to  overcome  the  contraction  of  their  antagonists,  which 
are  also  excited  to  action  during  the  voluntary  effort  to  contract  the 
paralyzed  group.  The  assistant  must  then  aid  the  paralyzed  muscles 
by  passively  extending  the  healthy  antagonist  muscles.  The  action  of 
the  healthy  antagonist  muscles  can  be  weakened,  not  only  by  the  hands 
of  an  assistant,  but  also  by  fixing  elastic  bands  or  spiral  wires  to  the 
limb  so  as  to  aid  the  action  of  the  paralyzed  groups.  In  the  Swedish 
system  great  attention  is  paid  to  the  development  and  strengthening 
of  the  extensors  of  the  body. 

Ordinary  gymnastic  exercises  are  also  useful  in  the  treatment  of 
various  nervous  affections.  By  their  use  the  nutrition  of  the  muscular 
system  is  improved,  the  heart  propels  the  blood  more  eflSciently  through 
the  organism,  the  blood  itself  becomes  of  better  quality,  and  the  nervous 
system  participates  in  the  general  improvement. 

Mechanical  Vibrations. — Some  years  ago,  Dr.  Mortimer  Granville 
was  led  to  try  the  effects  of  rapidly  tapping  the  skin  over  the  fiftli 
nerve  in  a  case  of  facial  neuralgia  by  means  of  a  Bennett's  percussion 
hammer,  using  the  pleximeter  as  a  shield.  The  results  obtained  were 
so  encouraging  that  he  gradually  extended  the  application  of  mechani- 
cal vibration  as  a  therapeutic  remedy  to  various  other  nervous  diseases. 
With  the  view  of  better  regulating  the  number  and  strength  of  the 


REMOVAL    OF    THE    ANATOMICAL    CAUSE.  231 

l)lows  which  can  be  delivered  in  a  given  time,  Dr.  Granville  had  an 
instrument  constructed  Avhich  he  names  "percuteur."  The  newest 
and  most  efficient  percuteur  is  worked  by  electricity,  but  it  is  important 
to  remember  that  no  electricity  passes  through  the  patient ;  the  elec- 
tricity is  converted  into  mechanical  motion,  and  its  only  use  is  to  enable 
the  performer  to  deliver  a  regulated  number  of  blows  on  any  desired 
l)art,  just  as  was  done  more  roughly  by  means  of  Bennett's  percussion 
hammer.  Dr.  Granville  believes  that  by  means  of  mechanical  vibra- 
tions he  can  relieve  a  considerable  number  of  cases  of  neuralgia ;  that 
much  amendment  occurs  by  its  use  in  the  early  stages  of  locomotor 
ataxia  and  lateral  sclerosis ;  and  that  by  it  he  can  even  arouse  torpid 
nerve  centres  to  action,  and  consequently  that  it  is  of  great  use  in  the 
treatment  of  neurasthenia. 

Electricity  in  the  forms  of  the  galvanic  and  induced  currents  is  one 
of  the  most  useful  remedies  we  possess  in  the  treatment  of  the  diseases 
of  the  nervous  system.  Only  the  briefest  possible  account  can  here  be 
given  of  the  methods  of  application  and  uses  of  electricity  in  the  treat- 
ment of  disease,  and  the  student  is  referred  for  further  information  to 
books  specially  devoted  to  this  subject,  the  valuable  work  of  Dr.  De 
Watteville  on  "Medical  Electricity"  being  particularly  recommended 
to  the  English  reader. 

In  selecting  the  position  upon  which  the  electrodes  are  to  be  placed, 
two  methods  of  application  have  been  adopted,  viz.,  the  direction  and 
poJcir  methods.  In  the  direction  method  one  rheophore  is  placed  over 
the  plexus  and  the  other  over  the  trunk  of  the  nerve.  When  the  posi- 
tive pole  or  anode  is  centrally  placed  the  current  is  called  a  deseending 
current,  and  Avhen  the  cathode  occupies  that  position  the  current  is 
called  an  ascending  current.  In  the  polar  method  one  rheophore  is 
placed  on  an  indifferent  part  of  the  body,  such  as  the  sternum,  and  the 
other  is  placed  over  the  nerve  or  muscle  which  it  is  desired  to  stimulate. 
It  does  not  appear  that  there  is  any  essential  diiference  in  principle 
between  these  two  methods.  When  the  cathode  is  used  as  the  exciting 
pole  in  the  polar  method,  the  same  kind  and  degree  of  contraction  is 
obtained  as  when  the  cathode  is  peripherally  placed  in  the  direction 
method ;  and,  conversely,  when  the  anode  is  used  as  the  exciting  pole 
in  the  polar  method,  the  reactions  obtained  are  the  same  as  those  pro- 
duced when  the  anode  is  peripherally  placed  in  the  direction  method. 
In  practice,  therefore,  it  appears  to  be  indifferent  whether  the  polar  or 
direction  method  be  employed,  but  those  positions  should  be  chosen 
Avhich  will  best  insure  that  the  tissue  or  organ  which  it  is  desired  to 
influence  shall  be  thoroughly  permeated  by  the  current.  With  refer- 
ence  to   the  size  of  the  electrodes,  the  general  rule  is  that,  when  a 


2-^2  GENERAL    TREATMENT. 

purely  local  effect  on  a  nerve  or  muscle  is  Avanted  for  diagnostic  pur- 
poses, the  electrodes  should  be  small ;  but  when  an  alterative  effect  on 
deeply  seated  organs  is  required  large  electrodes,  thoroughly  moistened, 
should  be  employed.  The  current,  instead  of  being  passed  through 
the  skin,  may  be  sent  directly  to  a  nerve  or  muscle  which  it  is  desired 
to  stimulate  by  means  of  needles  introduced  into  its  substance.  This 
method,  which  is  only  of  limited  application  in  therapeutics,  is  called 
electric  acupuncture. 

aalvanhation.— There  are  three  methods  of  applying  the  galvanic 
current,  according  as  it  is  desired  to  obtain  its  sedative,  alterative,  or 
stimulant  action.  According  to  the  first  method  the  rheophores  are 
maintained  immovable  on  the  skin,  or  the  affected  extremities  are  placed 
in  tepid  salt  water,  with  which  the  conducting  wires  of  the  battery  are 
in  contact.  This  is  the  stabile  method  of  application.  In  the  second 
or  labile  method  of  application  the  cathode  is  made  to  glide  over  the 
skin  in  the  direction  of  the  nerves  and  muscles  to  be  acted  on.  The 
third  or  interrupted  method  is  based  upon  the  fiict  that  the  constant 
current  acts  as  a  stimulus  to  both  nerves  and  muscles  at  the  moment  of 
making  and  breaking  contact.  In  using  this  method  one  pole  is  held 
immovable  on  one  point,  whilst  the  other  is  made  repeatedly  to  touch 
the  part  to  be  stimulated.  The  current  may  also  be  interrupted  by 
means  of  a  commutator.  A  still  more  powerful  effect  is  produced  l)y 
suddenly  reversing  the  direction  of  the  current  by  means  of  the  com- 
mutator— a  descending  current,  for  instance,  being  suddenly  changed 
for  an  ascending  current.  This  method  has  been  called  by  Remak, 
who  introduced  the  practice,  voltaic  alternatives. 

Faradization. — When  it  is  desired  to  limit  the  current  to  the  skin 
the  rheophores  must  be  used  dry,  and  the  skin  should  also  be  dusted 
with  toilet  powder  or  some  other  absorbent  powder  so  as  to  diminish  its 
conductivity.  The  electrode  used  should  be  metallic,  either  in  the  form 
of  a  cylinder,  disk,  or  wire  brush,  and  the  useful  method  of  application 
is  what  is  known  as  the  electric  hand.  A  moist  rheophore  is  applied 
over  the  sternum  or  other  indifferent  part  of  the  body,  and  the  other  is 
held  in  one  hand  of  the  operator  while  he  passes  the  back  of  the  dis- 
engaged hand  over  the  part  which  it  is  desired  to  excite.  When  the 
deeper  tissues  are  to  be  reached  through  the  skin  the  rheophores  should 
consist  of  well-moistened  sponges  in  cylinders,  or  metallic  disks  covered 
with  wet  leather,  and  the  skin  itself  should  be  thoroughly  moistened 
with  a  mixture  of  warm  water  and  salt.  In  order  to  electrize  a  muscle 
completely  the  rheophores  should  be  applied  over  its  fleshy  body,  and 
they  should  either  cover  its  whole  surfoce  or  be  applied  in  succession 
to  all  points  of  its  surface.     When  the  body  of  the  muscle   is   thick  a 


REMOVAL    OF    THE    ANATOMICAL    CAUSE.  288 

Strong  current  should  be  used  ;  otherwise  the  superficial  layers  alone 
are  excited.  The  easiest  way  to  apply  the  current  to  a  muscle  is  to 
hold  the  handles  of  the  rheophores  in  the  right  hand,  one  between  the 
thumb  and  index  finger,  and  the  other  between  the  middle  and  rino- 
fingers.  The  two  electrodes  are  then  moved  up  and  down  over  the 
whole  surface  of  the  muscle  so  as  to  secure  a  thorough  contraction  of 
every  part  of  it.  The  faradic  current  is  passed  through  a  nerve  in  order 
to  obtain  contraction  of  the  muscle  or  group  of  muscles  Avhich  it  sup- 
plies. The  polar  method  is  adopted  for  this  purpose,  one  electrode 
being  placed  over  the  sternum  or  some  indifferent  part  of  the  body, 
and  the  other  over  the  course  of  the  nerve  at  the  motor  points,  as  indi- 
cated in  Ziemssens  diagrams. 

Central  galvanization  aims  at  bringing  the  whole  of  the  central 
nervous  system  under  the  influence  of  the  current.  The  cathode  is 
held  immovable  over  the  epigastrium,  while  the  anode  is  passed  over 
the  forehead  and  top  of  the  head,  along  the  inner  border  of  the  sterno- 
mastoid,  over  the  course  of  the  pneumogastric  and  sympathetic  in  the 
neck,  over  the  nape  of  the  neck,  and  along  the  whole  length  of  the 
spine. 

G-cneral  faradization  aims  at  bringing  the  whole  muscular  system 
under  the  influence  of  the  current.  One  pole,  usually  the  negative,  is 
placed  on  some  insensitive  part  of  the  body  or  fixed  to  a  copper  plate 
upon  which  the  soles  of  the  feet  are  placed,  while  the  other  is  either 
sponged  over  the  whole  body  or  kept  stationary  at  certain  points. 

G-alvano-faradization  is  obtained  by  joining  the  induction  coil  and 
the  galvanic  battery  in  one  circuit.  The  negative  pole  of  the  one  is 
connected  by  means  of  a  wire  with  the  positive  of  the  other,  while  the 
electrodes  are  attached  to  the  two  extreme  poles.  I  have  had  repeated 
opportunities  for  observing  the  excellent  results  which  are  obtained  by 
this  method  in  the  practice  of  my  colleague.  Dr.  Morgan,  who  was  the 
first  to  devise  this  method.  Dr.  De  Watteville,  who  appears  to  have 
adopted  this  method  independently  of  Dr.  Morgan,  speaks  very  higlily 
of  its  power  as  a  therapeutic  agent. 

Uses  of  Electricity. — The  faradic  current  is  a  powerful  stimulant  to 
both  nerves  and  muscles,  and  when  a  simple  stimulant  effect  is  alone 
desired  this  current  is,  as  a  rule,  more  applicable  than  the  galvanic 
current.  This  current  may,  therefore,  be  used  as  a  stimulant  either  to 
act  on  the  skin  directly  in  cases  of  anaesthesia,  or  to  act  indirectly  on 
remote  organs  in  a  reflex  manner ;  or  it  may  be  used  as  a  jiowerful 
neuro-muscular  stimulant  in  the  various  forms  of  paralysis.  The  gal- 
vanic current  acts  as  a  stimulant  to  nerves  and  muscles  both  on  making 


234  GEXERAL    TREATMENT. 

and  breaking  contact,  and,  in  addition,  produces  a  profound  alteration 
of  nutrition  during  the  time  the  current  is  interruptedly  passing  through 
an  oro-an.  The  latter  action  has  been  called  by  Remak  its  catalytic 
action^nd  it  is  to  it  probably  that  the  constant  current  owes  the  many 
advantages  it  possesses  over  the  faradic  current  in  the  treatment  of 
many  of  the  diseases  of  the  nervous  system.  The  stimulant  action  of 
the  constant  current  is,  however,  very  important  both  as  a  means  of 
diao-nosis  and  in  the  treatment  of  paralysis.  We  have  seen  that  while 
paralyzed  muscles  manifest  the  reaction  of  degeneration,  they  are  more 
sensitive  to  the  action  of  the  galvanic  than  of  the  faradic  current,  and 
in  these  cases  the  constant  current  should  be  selected  to  stimulate  the 
nutrition  of  the  affected  muscles.  With  this  exception,  however,  the 
faradic  is  a  more  powerful  agent  in  the  direct  treatment  of  paralyzed 
muscles  than  the  constant  current.  But  the  catalytic  action  of  the 
constant  current  renders  it  an  exceedingly  valuable  agent  in  modifying 
the  nutrition  of  the  nerves  and  trunks  of  the  central  organs  of  the 
nervous  svstem,  and  it  may  even  be  used  in  the  treatment  of  cases 
where  the  irritaljility  of  portions  of  the  nervous  system  is  increased, 
and  to  which,  therefore,  the  faradic  current  is  wholly  inapplicable.  As 
examples  of  the  numerous  applications  of  the  constant  current  may  be 
mentioned  its  emi^oyment  for  the  relief  of  pain  in  neuralgia  and  the 
assuaging  of  various  forms  of  spasm,  not  to  speak  of  its  numerous 
applications,  both  locally  and  generally,  in  the  treatment  of  chronic 
diseases  of  the  brain,  spinal  cord,  special  senses,  and  viscera. 

4.  TO  ALLAY  OR  REMOVE  SERIOUS  SYMPTOMS. 

The  fourth  indication  of  treatment  is  to  allay  or  remove  serious 
symptoms,  and  of  these  the  distressing  symptom  of  pain  is  by  far  the 
most  prominent  and  important.  Opium  is  the  most  powerful  remedy 
Ave  possess  for  the  alleviation  of  pain,  and  it  acts  most  effectually  when 
administered  in  the  form  of  subcutaneous  injection  of  morphia.  Brom- 
ide of  potassium,  chloride  of  ammonium,  chloral  hydrate,  croton  chloral, 
atropia,  quinine,  and  various  other  agents  may  at  times  be  used  in  pref- 
erence to  opium  in  cases  of  neuralgia.  The  constant  current  is  also  a 
valuable  agent  for  assuaging  pain,  and  when  it  succeeds  it  should  be 
preferred  to  all  other  remedies,  inasmuch  as  its  use  is  unattended  by 
any  evil  after-consequences.  Cold,  continuously  applied,  has  been  used 
as  a  palliative  for  the  removal  of  pain  in  neuralgia,  while  at  other  times 
the  local  application  of  warmth  aff"ords  greater  relief,  acting,  probably, 
by  relaxing  the  tissues  in  which  the  nerve  fibres  are  embedded.      Con- 


TO    ALLAY    OK    REMOVE    SERIOUS    SYMPTOMS.  235 

tinuotis pju'ssiire  over  a  nerve  is  often  useful  in  neuralgia  and  in  cases 
of  motor  spasm,  the  action  being  produced  by  arrest  of  the  conduc- 
tion through  the  nerve.  Ointments  and  liniments  of  aconite,  veratrine, 
opium,  or  atropine  are  useful  as  local  applications  for  the  removal  of 
pain. 

Surgical  operations  have  been  successfully  undertaken  for  the  re- 
moval of  pain  or  spasm.  These  operations  are  performed  with  the 
view  of  arresting  the  conduction  of  nerves  in  cases  of  neuralgia  or  in 
local  spasms.  The  operations  are  neurotomy,  in  which  the  nerve  is 
simply  divided ;  neurectomy,  in  which  a  portion  of  it  is  dissected  out ; 
and  nerve -stretching,  in  which  the  nerve  is  powerfully  stretched.  The 
conditions  under  which  each  of  these  operations  ought  to  be  under- 
taken, will  be  mentioned  in  another  part  of  this  work. 


V 

f 

i 


SPECIAL  PATHOLOGY  OF  THE  NERVOUS  SYSTEM. 


CHAPTER    I. 

GENERAL  DISEASES  OF  THE  PERIPHERAL  NERVES. 

1.   HYPEE.EMIA  OK  CONGESTION  OF  THE  NERVES. 

CoxcESTiox  of  the  nerves  is  caused  by  exposure  to  great  cold,  as 
lias  been  proved  by  S.  Weir  Mitchell,  who  found  that  exposed  nerves 
■which  had  been  frozen  became  congested  and  SAvollen  on  thawinii-. 

Sy)iq}toms. — The  symptoms  caused  by  freezing  of  nerves  were  first 
studied  by  Waller,  who  froze  the  ulnar  nerve  by  placing  the  elbow  in  a 
freezing  solution.  The  first  symptoms  are  pain,  anaesthesia,  paralysis, 
and  increase  of  temperature  in  the  region  of  chstribution  of  the  nerve. 
In  the  thawed  portion  a  very  painful  sensation  is  felt  which  spreads 
backwards  to  the  brachial  plexus,  and  may  even  produce  vertigo  and 
faintness.  The  symptoms  wliich  follow  the  thawing  of  the  nerve  are 
hyperi^sthesia,  numbness,  formication,  and  partial  loss  of  power,  but 
no  elevation  of  temperature  in  the  area  of  distribution  of  the  aflected 
nerve. 

2.  INFLAMMATION   OF  NEEVES— NEURITIS  AND  PERINEURITIS. 

Etiohiiy. — Inflammation  of  peripheral  nerves  is  caused  by  wounds, 
contusions,  rupture,  laceration,  or  sudden  compression  of  the  nerve,  or 
by  exposure  to  cold  and  wet.  Neuritis  may  also  be  caused  by  exten- 
sion of  inflammation  from  the  surrounding  tissues  and  organs.  The 
most  notable  diseases  which  set  up  neuritis  are  caries  of  bones,  inflamed 
tendinous  sheaths,  acute  and  chronic  inflammation  of  joints,  abscesses, 
and  malignant  growths.  It  is  also  frequently  developed  after  acute 
diseases  such  as  the  acute  exanthemata,  typhoid  fever,  and  diphtheria, 
and  after  chronic  diseases  like  rheumatism  and  syphilis.  Inflammation 
of  nerves  is  also  met  with  in  lepra  an;\?sthetiea,  herpes  zoster,  and  van- 


238      GENERAL  DISEASES  OF  THE   PERIPHERAL   NERVES. 

ous  other  cutaneous  affections,  and  it  may  appear  in  the  absence  of  any 
recognizable  cause,  being  then  called  idiopathic  neuritis. 

Symptoyns. — The  symptoms  of  neuritis  differ  according  as  the  in- 
flammation is  (a)  acute  or  {h)  chronic. 

[a)  Acute  neuritis  comes  on  soon  after  exposure  of  the  nerve  to  one 
or  other  of  the  causes  of  the  disease.  It  is  ushered  in  by  a  well- 
marked  feeling  of  chilliness,  or  by  an  actual  rigor,  which  is  accom- 
panied by  headache,  sleeplessness,  and  smart  fever.  In  inflammation 
of  a  mixed  or  sensory  nerve  the  patient  experiences  a  severe  and  almost 
intolerable  pain  in  the  region  of  the  affected  nerve,  and  Avhich  often 
radiates  into  the  areas  of  other  branches  of  the  same  plexus,  or  into 
more  remote  nerve  territories.  The  pain  is  deep-seated,  tearing,  boring, 
or  burning,  and  it  is  described  as  being  almost  continuous,  although 
there  may  be  remissions  and  paroxysmal  exacerbations,  the  latter 
being  specially  apt  to  occur  at  night.  Every  movement  of  the  limb 
augments  the  sufferings  of  the  patient,  and  pressure  over  the  affected 
nerve  causes  intense  pain,  which  radiates  from  it  in  all  directions.  The 
tract  of  the  inflamed  nerve  is  sometimes  indicated  by  a  red  line  like  that 
which  occurs  in  inflammation  of  a  superficial  lymphatic  vessel.  I'he  skin 
over  the  whole  area  of  distribution  of  the  nerve  is  at  first  extrenielV"  sen- 
sitive to  the  slightest  contact,  and  the  patient  complains  of  numbness 
and  formication  of  this  area,  but  the  hyperesthesia  soon  gives  place  to 
anaesthesia.  In  the  early  stage  of  the  disease  muscular  spasms  and 
twitchings  may  be  present,  but  these  are  soon  replaced  by  paralysis  of 
the  muscles  supplied  by  the  nerve.  The  degree  of  paralysis  varies 
according  to  the  severity  of  the  inflammation,  but  in  all  aggravated 
cases  the  muscles  undergo  rapid  atrophy,  and  manifest  "the  reaction  of 
degeneration."  In  excitable  patients  an  attack  of  acute  neuritis  may  be 
attended  by  slight  delirium,  and  an  emotional  condition  is  sometimes 
induced  which  may  be  mistaken  for  an  attack  of  hysteria. 

(h)  Chronic  neuritis  occurs  either  as  a  sefjuel  of  an  acute  attack,  or 
it  arises  insidiously  with  obscure  symptoms,  which  gradually  or  sud- 
denly attain  great  intensity.  Pain  is  the  earliest  and  most  constant 
symptom ;  it  varies  considerably  in  character  and  intensity,'  being  some- 
times dull  and  tensive,  at  other  times  of  a  lancinating,  tearing  char- 
acter, and  radiating  towards  the  periphery.  The  pain  is  continuous, 
although  it  is  frequently  interrupted  by  paroxysmal  exacerbations, 
which  generally  occur  at  night  and  prevent  sleep.  It  is  increased  by 
every  kind  of  exertion  and  movement,  and  by  everything  which  excites 
the  activity  of  the  heart.  In  the  first  stages  of  the  disease  the  patient 
complams  of  numbness  an(J  of  formication,  and  of  unpleasant  pricking 
sensations  when  the  skin  is  touched  or  struck,  but  in  the  later  stages  of 


ATROPHY    OF    NERVES.  239 

the  disease  anaesthesia  is  established,  which  may  vary  in  degree  from  a 
slight  blunting  of  sensibility  up  to  complete  loss  of  all  forms  of  sensi- 
bility. 

Symptoms  of  motor  irritation,  such  as  tension,  sudden  contractions, 
cramps,  or  persistent  contractures  of  the  muscles,  are  present  in  the 
early  stage  of  the  disease,  but  these  are  succeeded  by  paralytic  phe- 
nomena. Tlie  muscular  spasms  are  sometimes  direct  and  sometimes 
reflex.  Reflex  spasms  are  met  with  in  the  facial  muscles  when  the 
fifth  nerve  is  affected,  and  the  sphincter  of  the  iris  and  ciliary  muscle 
may  be  the  subjects  of  spasm  when  the  ophthalmic  branch  is  impli- 
cated ;  and  even  in  neuritis  of  mixed  nerves  reflex  spasms  are  some- 
times so  violent  that,  for  example,  the  finger-nails  may  become  buried 
in  the  skin  of  the  palm  from  spasm  of  the  flexors. 

The  affected  nerve  is  swollen,  and  when  it  occupies  a  superficial 
position  it  can  be  felt  as  a  continuously  thick  cord.  In  other  cases  the 
thickening  occurs  at  certain  intervals,  and  then  fusiform  or  moniliform 
swellings  may  be  felt  in  the  course  of  the  nerve — a  condition  which 
has  been  named  neuritis  nodosa.  The  nerve  is  always  sensitive  to 
pressure,  and  compression  of  the  swollen  portions  gives  rise  to  eccentric 
pains  and  formication. 

The  electrical  reactions  of  the  affected  nerves  and  muscles  may 
remain  normal  or  be  even  increased  in  slight  cases ;  but  in  rheumatic 
and  syphilitic  cases,  and,  indeed,  in  all  aggravated  forms  of  the  disease, 
the  muscles  undergo  atrophy  and  manifest  the  "  reaction  of  degenera- 
tion." 

Trophic  disorders  of  the  skin  and  nails  and  swelling  and  stiffiiess 
of  the  joints  are  frequently  observed  in  chronic  neuritis ;  hysterical 
or  epileptic  convulsions  and  tetanus  frequently  result  from  neuritis. 

3.  ATEOPHY  OF  NEEVES. 

Atrophy  of  nerves  may,  as  we  have  already  seen,  be  con<ienital  in 
those  cases  where  portions  of  the  body  are  incompletely  formed,  idio- 
pathic when  there  is  a  simple  wasting  of  the  nerve  fibres,  as  occurs  in 
atrophy  of  the  optic  nerves  in  tabes  dorsalis,  and  secondary  when  the 
nerve  fibres  are  separated  from  their  trophic  centres. 

Symjotoms. — It  may  be  laid  down  as  a  general  rule  that  whenever 
atrophy  of  a  nerve  exists  its  function  is  lowered  or  lost.  Secondary 
atrophy  of  motor  nerves  may  be  distinguished  by  electrical  examina- 
tion, and  primary  atrophy  of  the  optic  nerves  may  be  recognized  by 
an  ophthalmoscopic  examination. 


■940      GENERAL   DISEASES  OF   THE   PEKIPHERAL   XERVES. 

4.  HYPERTROPHY  OF  NERVES. 

Hvpertropliy  of  nerves  is  a  mere  anatomical  curiosity,  and  is  not 
known  to  be  connected  with  any  definite  symptoms. 

5.  NEUROMATA. 

Etiolof/i/. Some  individuals  appear  to  be  predisposed  to  the  forma- 
tion of  neuromata,  and  phthisical  and  scrofulous  persons  seem  to  be 
particularly  liable  to  their  formation.  Isolated  neuromata  are  more 
common  in  women  than  in  men,  while  multiple  neuromata  are  almost 
exclusively  met  with  in  men.  They  occur  at  all  ages,  and  are  often 
congenital. 

The  best  known  of  the  exciting  causes  are  blows,  intermittent  press- 
ure, penetration  and  retention  of  foreign  bodies,  and  various  injuries. 
JS'euromata  are  also  frequently  found  in  the  cicatrices  formed  after  nerves 
have  been  divided  or  injured,  and  swellings  of  the  ends  of  the  nerves 
.are  often  met  with  in  the  stumps  of  amputated  limbs.  Chronic  neu- 
ritis, syphilis,  lepra,  and  elephantiasis  may  lead  to  the  formation  of 
tumors  in  nerves,  and  in  a  large  number  of  cases  no  definite  cause  can 
.be  traced. 

Syinptoms. — The  symptoms  of  neuromata  are  variable,  many  of  them 
being  quite  painless,  and  others  causing  intense  and  persistent  suftering. 
Isolated  neuromata  give  rise  to  severe  and  incurable  neuralgia,  and 
they  have  consequently  been  called  tubcrrula  dolorosa.  The  pain  may 
be  tearing,  lancinating,  aching  boring,  or  burning ;  it  is  almost  always 
remittent  or  completely  intermittent,  but  when  the  paroxysm  comes  on 
the  pain  gradually  increases  in  intensity,  and  radiates  from  certiiin 
points  towards  the  periphery.  The  })ain  is  increased  by  cohl  and  <lanip 
weather,  by  pressure,  or  the  slightest  movement  of  the  affected  limb, 
and  in  women  frequently  by  the  return  of  the  menses  or  by  pregnancy. 
It  may  often  be  made  to  disappear  temporarily  by  firm  pressui-e  on  the 
nerve  above  the  tumor.  The  pain  is  generally  more  severe  in  small 
tumors  of  cutaneous  branches  than  in  larger  tumors  of  deeper  nerve- 
trunks.  In  addition  to  pain,  feelings  of  numbness  and  formication, 
and  sensations  of  heat  or  cold,  are  often  felt  in  the  area  of  distribution 
of  the  afiected  nerve.  In  some  cases  aniiesthesia  may  be  present,  and 
appears  not  infrequently  in  the  form  of  ancesthesia  dolorosa. 

Motor  disorders  are  rare,  but  sometimes  occur  in  the  form  of  tremors, 
spasms,  and  contractures,  and  these  may  ultimately  give  place  to  com- 
plete paralysis.  The  course  of  the  disease  is  very  variable.  True 
neuromata  may  remain  stationary  for  many  years  without  causing  any 


1 


NEUROMATA.  241 

serious  symptoms,  and  multiple  neuromata  are  sometimes  so  free  from 
l)ain  tliat  they  are  only  discovered  accidentally  during  life  or  at  the 
autopsy.  In  other  cases  active  symptoms,  present  for  a  time,  may 
remit  and  ultimately  cease,  and  in  a  few  cases  the  tumor  disappears. 
In  other  cases  the  tumor  gives  rise  to  persistent  paralysis,  and  tumors 
of  the  Cauda  equina  cause  anaesthesia  of  the  lower  extremities  of 
variable  distribution,  paraplegia,  and  various  trophic  disorders.  In 
other  cases  the  symptoms  are  such  as  to  give  rise  to  the  greatest  suffer- 
ing, and  to  cause  sleeplessness,  cachexia,  and  even  death  from  ex- 
haustion. 

Treatment. — The  treatment  must  be  directed  to  remove  the  cause, 
and  surgical  interference  is  frequently  necessary  in  cases  of  injury. 
At  other  times  the  treatment  must  be  directed  against  articular 
rheumatism,  inflammation  of  tendons,  syphilis,  and  other  morbid  con- 
ditions. 

In  simple  connestion  the  steady  application  of  ice  along  the  track  of 
the  nerve,  elevation  of  the  part,  and  absolute  rest  suffice  to  arrest  the 
disease. 

In  aciiti'  neuritis  energetic  antiphlogistic  treatment  nnist  be  a<lopted. 
consisting  of  local  dei)l('tion,  application  of  ice,  purgatives,  favorable 
position  of  the  parts,  and  absolute  rest.  Large  doses  of  quinine  may 
prove  useful,  and  large  doses  of  morphia  or  atropia  are  necessary  to 
allay  pain. 

In  suharute  and  clironic  neuritis  cold  may  be  applied  in  the  first 
stages,  but  depressing  treatment  must  soon  be  changed  for  counter- 
irritation  by  means  of  the  faradic  brush,  painting  with  iodine,  or  blis- 
tering. In  very  chronic  and  obstinate  cases  recourse  may  be  had  to 
energetic  counter-irritants,  such  as  the  moxa  and  the  actual  cautery. 
Hot  baths,  such  as  those  of  Wilbad,  Gastein,  Teplitz,  and  Wiesbaden, 
as  well  as  mud  and  strong  saline  baths,  have  been  found  useful  in  the 
treatment  of  chronic  neuritis.  The  galvanic  current  is  a  most  effectual 
remedy,  and  the  best  method  of  applying  it  appears  to  be  the  steady 
application  of  the  anode  for  a  few  minutes  each  day,  over  the  affected 
spot.  In  severe  cases  the  part  must  be  kept  at  absolute  rest  in 
an  appropriate  position,  and  the  patient  should  be  warned  against 
taking  active  exercise,  or  exposing  himself  to  cold  and  wet.  When  all 
active  symptoms  have  subsided  the  return  of  motion  to  paralyzed  mus- 
cles may  be  promoted  by  massage  and  the  faradic  current. 

In  congenital  atrophy  no  treatment  is  of  any  avail,  and  in  idioi)athic 
atrophy  a  simple  delay  in  the  progress  of  the  disease  is  all  that  can  be 
expected    from  treatment.     Secondary  atrophy  may  be  arrested,  and 

16 


2-i2      GENERAL  DISEASES  OF   THE   PERIPHERAL  XERVES. 

even  complete  recovery  may  take  place,  provided  the  primary  disease 
can  be  removed. 

The  only  successful  treatment  of  neuromata  is  afforded  by  the  ex- 
tirpation or  the  destruction  of  the  tumor.  Extirpation  succeeds  best 
when  the  growth  can  be  removed  whilst  the  nerve  is  left  intact.  When 
extirpation  is  impracticable  the  tumor  may  be  destroyed  by  caustics  or 
electrolysis,  but  these  methods  are  not  very  successful.  "When  the 
tumor  cannot  be  removed,  palliative  treatment  to  alleviate  the  suffer- 
ings of  the  patient  must  be  adopted. 


CHAPTER    II. 

DISORDEES  OF  COMMON  SENSATION  AND  OF  SPECIAL 

SENSE. 

I.  ANAESTHESIA  AND  ANALGESIA  IN  THE  REGION  OF  DISTEI- 
BUTION  OF  INDIVIDUAL  NERVES  AND  PLEXUSES. 

AVhen  a  purely  sensory  or  mixed  nerve  is  divided  a  certain  degree 
of  anaesthesia  is  generally  produced  in  the  cutaneous  area  supplied  by 
it,  but  the  extent  and  degree  of  this  anesthesia  are  very  variable,  and 
by  no  means  correspond  with  the  anatomical  distribution  of  the  sensory 
filaments  of  the  nerve.  Arloing  and  Tripier  found  that  section  of  one 
of  the  four  nerve  branches  by  which  the  digit  of  a  dog  or  cat  is  sup- 
plie<l  caused  no  recognizable  diminution  of  its  cutaneous  sensibility, 
section  of  two  branches  caused  only  slight  general  diminution  of  sensi- 
bility, section  of  three  branches  caused  decided  diminution  of  sensibility, 
but  complete  amTesthesia  of  any  part  of  the  digit  was  only  estaldished 
when  the  four  branches  were  divided.  They  also  found  that  on  the 
fifth  digit  of  the  dog,  which  is  supplied  from  branches  from  the  ulnar 
and  radial  nerves,  partial  anaesthesia  only  is  caused  by  section  of  one  or 
other  of  these  nerves,  while  on  the  fifth  digit  of  the  cat,  which  is  sup- 
plied by  branches  of  the  ulnar  nerve  alone,  section  of  the  nerve  caused 
complete  anoesthesia.  It  would  seem,  therefore,  that  the  skin  is  not 
mapped  out  into  functionally  independent  territories  corresponding  to 
the  anatomical  distribution  of  the  filaments  of  the  sensory  nerves. 
This  functional  intercommunication  between  neighboring  nerve  terri- 
tories is  explained  by  the  free  anastomosis  which  is  known  to  take 
place,  first,  between  branches  of  different  nerves  of  considerable  size, 
and  second,  between  those  nerves  in  the  terminal  networks  described 
by  Jacobowitsch  and  Beale.  Arloing  and  Tripier  have  described  a 
third  method  by  means  of  which  nerve  fibres  from  one  nerve  district 
may  be  distributed  to  another  territory.  After  division  of  one  of  the 
branches  of  the  median  nerve  of  the  dog  or  cat,  for  instance,  they 
found  that  the  animal  gave  manifest  evidence  of  pain  when  the  periph- 
eral portion  of  the  divided  branch  was  pinched,  and  even  division  of 
the  whole  nerve  did  not  entirely  prevent  these  manifestations  of  sensi- 
bility. The  peripheral  portion  of  the  divided  branch  was  cut  out  and 
examined  microscopically  a  few  days  after  section,  and  it  was  found 


I 


244  DISORDERS    OF    MIXED    NERVES. 

that  although  by  far  the  greater  number  of  fibres  were  degenerated, 
yet  a  few  of  them  had  remained  healthy.  A  portion  of  the  proximal 
end  of  the  divided  nerve  was  also  examined  microscopically,  and  a  few 
degenerated  fibres  were  discovered  amongst  a  large  number  of  healthy 
ones.  From  these  observations  the  authors  concluded  that  the  few 
fibres  which  remained  healthy  in  the  peripheral  portion  of  the  nerve 
still  retained  their  connection  with  their  trophic  centres,  while  the  few 
which  were  degenerated  in  the  proximal  portion  were  .severed  from 
their  centres.  As  the  trophic  centres  of  these  fibres  must  have  been 
situated  in  the  spinal  ganglia  or  in  the  gray  matter  of  the  cord,  they 
must  have  reached  the  divided  branch  from  the  peripheral  side  of  the 
point  of  section,  and  have  been  pursuing  a  centripetal  course,  and  the 
authors  justly  assume  that  these  fibres  conferred  recurrent  sensibility 
upon  the  peripheral  part  of  the  nerve.  They  also  believe  that  these 
fibres,  after  ascending  a  short  distance  in  the  nerve,  are  distributed  to 
the  skin,  and  tlms  take  an  important  part  in  supplying  one  district 
with  nerve  fibres  from  neighboring  nerve  territories.  It  has  also  been 
suggested  by  Jacobi  that  the  spinal  ganglia  form  a  centre  in  which  an 
anastomosis  takes  place  between  fil)res  from  different  cutaneous  nerve 
territories.  But  whether  these  explanations  be  satisfactory  or  not,  it  is 
at  least  certain  that,  after  division  of  a  principal  nerve  trunk,  complete 
angesthesia  is  either  absent  or  is  limited  to  a  very  small  portion  of  skin, 
while  the  area  of  partial  anaesthesia  is  much  less  than  that  of  the  ana- 
tomical distribution  of  the  sensory  branches  of  the  nerve.  A  detailed 
description  of  the  distribution  of  ansesthesia  in  diseases  and  injuries  of 
individual  nerves  will  be  given  when  we  come  to  discuss  paralysis  of 
peripheral  nerves,  because  the  presence  of  anesthesia  serves  to  distin- 
guish peripheral  paralysis  from  the  atrophic  paralysis  of  spinal  origin. 
The  distribution  of  angesthesia  in  disease  of  individual  nerves  may  also 
be  gathered  in  a  general  way  from  the  distribution  of  neuralgia  of  the 
same  nerves,  and  it  is  therefore  unnecessary  to  pursue  the  subject 
further  at  present. 

II.    HYrEK^ESTHESIA  AND  HYPERALGESIA    IN    THE    REGION    OF 
DISTRIBUTION  OF  INDIVIDUAL  NERVES  AND  PLEXUSES. 

The  most  characteristic  feature  of  the  hyper?esthesia  and  hyperal- 
gesia caused  by  disease  of  peripheral  nerves  is  that  they  are  apt,  by 
radiating  to  neighboring  nerve  territories,  to  extend  over  a  much  wider 
area  than  the  anatomical  distribution  of  the  sensory  branches  of  the 
affected  nerve.  The  distribution  of  hypernesthesia  in  disease  of  indi- 
vidual nerves  may,  however,  be  gathered  from  the  distribution  of  the 
pain  in  neuralgia  without  further  description. 


XKUHALGIA    OF   IXDIVIDUA].   XEEYES   AXD   PLEXUSES.      245 

III.   NEURALGIA   IN  THE  KEGION  OF  DISTKIBUTION  OF 
INDIVIDUAL  NERVES  AND  PLEXUSES. 

1.    NElRALlilA    OF    THE    FlFTH    NeRVE    (TRKiEMIXAL    NeURAL(;IA). 

Etiology. — Trigeminal  neuralgia  occurs  with  unusual  frequency  in 
epileptic  families,  and  in  the  female  sex.  The  passage  of  the  nerve 
through  long  bony  canals  renders  it  liable  to  be  implicated  in  various 
aflections  of  the  bones  and  periosteum.  Aneurism  of  the  internal 
carotid  artery,  exostoses  of  the  petrous  portion  of  the  temporal  bone, 
and  tumors  at  the  base  of  the  skull  give  rise  to  intractable  neuralgia 
by  pressure  on  the  Casserian  ganglion,  or  on  the  nerve  itself.  The 
important  special  causes  of  facial  neuralgia  are  peripheral  irritations, 
such  as  the  presence  of  carious  teeth,  retarded  appearance  and  false 
development  of  the  wisdom  teeth,  disease  of  the  nasal  and  frontal 
sinuses,  and  overexertion  of  the  eyes.  It  may  also  be  caused  by  remote 
irritation,  such  as  that  caused  by  intestinal  worms,  genital  excitement, 
and  uterine  disease,  or  may  result  from  injury  of  other  nerves,  exces- 
sive mental  strain,  and  emotional  disturbance.  The  ophthalmic  branch 
of  the  nerve  is  more  liable  than  any  other  nerve  to  malarial  neuralgia. 
Ani>?mia,  arterial  degeneration,  wounds,  cicatrices,  and  diseases  of 
neighborini:  tissues  exercise  the  same  influence  in  neuralgia  of  the  fifth 
as  in  the  neuralgine  of  other  nerve  territories. 

SymjJtoniH. — Facial  neuralgia  consists  of  attacks  of  pain  in  the  area 
of  distribution  of  the  fifth  nerve  (Fig.  77)  or  of  one  of  its  branches, 
which  are  apt  to  recur  on  the  slightest  exposure  to  the  exciting  cause, 
or  even  in  the  absence  of  such  cause.  Each  attack  is  made  up  of 
recurring  paroxysms  of  severe  pain,  separated  by  intervals  of  com- 
parative but  not  entire  freedom  from  pain.  The  actual  outburst  of 
severe  pain  may  be  preceded  by  obscure  feelings  of  discomfort,  itching 
or  formication  in  the  side  of  the  face,  flying  pains  about  the  teeth,  or 
by  a  feeling  of  general  malaise  and  shivering,  but  at  other  times  a 
severe  dart  of  pain  shoots  along  the  course  of  one  of  the  branches  of 
the  nerve  without  being  preceded  by  any  warning. 

Each  paroxysm  consists  of  a  succession  of  quick  lightning-like  darts 
of  pain,  which  emanate  from  one  or  two  foci  and  radiate  toAvards  the 
[)eriphery.  At  first  one  or  two  of  these  flashes  may  be  followed  by  a  com- 
paratively free  interval,  but  they  recur  with  increasing  severity  and 
(juickness,  until  they  at  last  blend  into  an  uninterrupted  pain  of  great 
intensity,  during  the  continuance  of  which  the  patient  sufters  indescrib- 
able agony.     After  one  or  two  minutes  the  intensity  of  the  shooting  pain 


246 


DISOKDERS    OF    MIXED    NERVES, 


abates,  but  the  patient  continues  to  suffer  during  the  interval  from  a 
dull  achinc^  pain,  which  occasions  great  discomfort  and  prevents  sleep. 
The  character  of  the  pain  during  the  paroxysm  varies ;  it  may  be 
burning,  boring,  cutting,  crushing,  or  stabbing,  although  the  lightning- 
like  shocks  are  most  frequently  met  with.  The  intensity  of  the  disease 
may  vary  from  an  attack   which  consists  of  a  few  darts  of  pam  or  a 

Fig.  77. 


Skn^ory  Nerves  of  the  Head  and  Face.     (At'ter  Fi.oweu.) 


First  division  of  the  fifth  : 

SO,  Supraorbital. 

ST,  Supratrochlear. 

IT,  Infratrochlear. 

L,  Lachrymal. 

N,  Nasal. 
Second  division  of  the  fifth  : 

10,  Infraorbital. 

T3I,  Temporo-malar. 


Third  division  of  the  fifth  : 

B,  Buccal. 

M,  Mental. 

AT,  Auriculo-teniporal. 
Branches  of  the  cervical  plexus 

GO,  Great  occipital. 

S'O',  Small  occipital. 

GA,  Great  auricular. 

SC,  Superficial  cervical. 

IIIC,  Third  cervical. 


little  tinghng  of  the  face,  and  manifests  no  tendency  to  recur,  up  to 
a  disease  of  the  most  obstinate  character,  that  recurs  repeatedly  and 
with  great  severity  during  the  whole  of  life,  and  in  which  an  attack 
may  be  determined  by  such  a  slight  exciting  cause  as  a  current  of  cold 
air  on  the  cheek,  or  such  actions  as  chewing,  coughing,  washing  the 
face,  or  slight  emotional  disturbances. 

Painful  points  are  observed  during  the  attacks,  and  sometimes  even 
in  the  periods  of  intermission,  corresponding  generally  to  the  localities 
Avhere  the  nerve  becomes  more  superficial,  either  in  issuing  from  a  bony 
canal  or  in  penetrating  fascias. 


NEURALGIA   OF   INDIVIDUAL  NERVES  AND   PLEXUSES.      247 

The  ronroinitant  symptoms  of  trigeminal  neuralgia  are  very  numer- 
ous. During  a  severe  paroxysm  the  pain  often  radiates  to  other  nerve 
territories,  extending  to  the  other  branches  of  the  fifth,  when  one  only 
is  primarily  affected,  or  to  the  occipital,  cervico-brachial,  or  intercostal 
sensory  nerves.  The  skin  is  generally  hypersesthetic  in  the  early 
stages  of  the  disease,  and  often  anaesthetic  in  chronic  cases.  Disturb- 
ances of  special  sense  have  occasionally  l^een  observed  in  facial  neural- 
gia, consisting  of  photophobia,  amblyopia,  or  even  amaurosis,  and  dis- 
orders of  the  senses  of  hearing,  tasting,  and  smellino-. 

Motor  disorders  are  almost  always  present  in  aggravated  cases,  and 
consist  of  clonic  and  tonic  spasms  of  all  the  muscles  of  the  affected  side 
of  the  face,  or  of  a  few  only  of  them,  such  as  those  of  the  eyelid  or 
the  angle  of  the  mouth,  while  the  muscles  of  mastication  and  of  the 
tongue  are  sometimes  attacked. 

Vaso-motor  disturbances  are  manifested  by  pallor  and  coldness  in 
the  early  stage  of  the  attack,  but  these  are  quickly  followed  by  intense 
redness  and  elevation  of  temperature,  and  then  the  skin  1)ecomes  glossy 
and  oedematous.  The  redness  extends  to  the  mucous  membranes  sup- 
plied by  the  affected  nerve,  the  conjunctiva  being  specially  liable  to 
become  red  and  congested;  the  carotid,  facial,  and  temporal  arteries  of 
the  affected  side  may  be  seen  to  pulsate  strongly,  and  the  side  of  the 
face  is  covered  by  beads  of  perspiration. 

Seeretory  disorders  are  represented  by  an  increased  flow  of  tears, 
by  arrest  or  increase  of  the  secretion  of  the  mucous  membrane  of  the 
nose,  and  occasionally  by  augmented  salivary  secretion. 

The  tropldc  disturbances  consist  of  swelling  of  the  face,  changes  in 
the  color  and  texture  of  the  hair,  herpes  zoster  frontalis,  erysipelas, 
subacute  inflammation  of  the  periosteum  and  of  the  fibrous  membranes 
in  the  neighborhood  of  the  painful  points,  neuroparalytic  ophthalmia, 
iritis,  and  glaucoma.  In  aggravated  and  long-continued  cases  the  inces- 
sant pain  and  its  attendant  sleeplessness  undermine  the  constitution, 
the  general  nutrition  becomes  impaired,  and  at  last  the  patient  suffers 
from  marasmus  and  nervous  exhaustion. 

The  psychical  disorders  present  are  mental  irritability  and  despon- 
dency, and  hysterical  seizures,  whilst  occasionally  patients  have  com- 
mitted suicide  to  escape  from  their  sufferings. 

Varieties  of  Trifjeminal  Neuralgia, 
a.  Ophthalmic  or  Supraorbital  Neuralgia. 

In  this  form  several  branches  of  the  first  division  of  the  fifth  nerve 
(Fig.  78)  are  all  aftected,  or  the  pain  is  limited  to  some  particular 
branch. 


248 


DISORDERS    OF    MIXED    NERVES. 


The  painful  points  are  : 

(1)  The  supraorbital  point,  at  or   near  the  supraorbital  foramen : 
(2)  the  palpebral,  in  tlie  upper  eyelid ;  (3)  the  nasal,  at  the  point  of 


Fig.  78. 


DiAfiRAM   OF   THE   FiRST   AND   SfxOND    (SUPERIOR   MaXILLARY)    DIVISIONS   OF   THE    KlFTH    XeRVE,    ITS 

Connections  and  Chief  Branches.     (From  Hermann's  "  Phj'siology.") 
V,  Placed  over  Casserian  ganglion. 

a,  First  or  ophthalmic  division,  with  d  its  frontal,  e  its  lachnjmnl,  and/  its  miml  branches 
6,  Second  or  superior  maxillary  division,  branches  of  wlilch  are  marked  as  follows  : 

1,  Its  terminal  branches,  nasal,  labial,  and  palpebruL 

2,  Itecurrent  branch  to  the  ckira  mater,  and  middle  metdiujeid  artery. 

3,  Oibital  branch. 

4  is  placed  between  the  two  spheuo-palatiue  branches  (which  descend  to  Meckel's  ganglion) 
.5,  Dental  branches. 
MG,  Meckel's  ganglion. 

6,  The  Vidian  nerve  (constituting  the  motor  and  sympathetic  root  of  Jleckel's  ganglion). 

7,  The  ijreat  svperficinl  pttruml  nerve,  from  the  geniculate  ganglion  of  the  facial  nerve,  joining 

the  Vidian. 

8,  The  sympatlu'lic  branch  from  the  plexus  on  the  carotid  artery,   joining  the  ijreat  sKperficial 

petrosal,  and  forming  with  it  the  Vidian  nerve 

9,  Ascending  branches  of  Meckel's  ganglion. 

10,  Descending  palatine  branches. 

11,  Naso-palatine  branch. 

12,  Upper  nasal  branches. 

13,  Pharyngeal  liranch 

F,  Facial  nerve.     CA,  Carotid  artery.     IF,  Infraorbital  foramen. 


emergence  of  the  long  nasal  branch  at  the  junction  of  the  nasal  bone 
with  the  cartilage ;  (4)  the  ocular,  a  some-what  indefinite  focus  'vvithin 


NEURALGIA   OF   INDIVIDUAL   NERVES   AND   PLEXUSES.      249 

the  globe  of  the  eye  when  the  ciliary  nerves  are  aftected ;  (5)  the 
trochlear,  at  the  inner  angle  of  the  orbit.  The  characteristic  features 
of  ophthalmic  neuralgia  are  pain  in  the  forehead,  extending  down-^-ards 
to  the  upper  eyelid  and  root  of  the  nose,  hyperemia  of  the  conjunctiva, 
lachrymation,  and  a  painful  spot  at  the  supraorbital  foramen.  Malarial 
neuralgia  almost  ahvays  assumes  this  form ;  the  attacks  recur  with 
great  regularity,  and  are  very  intense. 

b.  SUPRAMAXILLARY    NEURALGIA. 

"When  all  the  branches  of  the  second  division  of  the  fifth  nerve 
(Fig.  78)  are  affected  the  pain  is  situated  in  the  cheek,  eyelid,  lateral 
portion  of  the  nose  and  upper  lip  (infraorbital  nerve),  in  the  zygomatic 
arch  and  anterior  temporal  region  (orbital  nerve),  in  the  upper  row  of 
teeth  (dental  branches),  and  in  the  nasal  cavities  and  gums  (naso-pala- 
tine  and  posterior  palatine  nerves). 

Infraorbital  neuralgia  is  the  most  common  variety  of  the  second 
division  of  the  nerve,  and  the  characteristic  pain  is  localized  in  the 
cheek,  upper  lip,  upper  row  of  teeth,  and  the  neighborhood  of  the 
zygomatic  arch.  An  ol)stinate  form  of  neuralgia  has  been  described 
by  Gross  which  appears  to  have  its  seat  in  the  remnants  of  the  alveolar 
processes  or  the  overlying  gum  in  elderly  persons  who  have  lost  their 
teeth. 

The  painful  points  of  supramaxillary  neuralgia  are :  (1)  The  infra- 
orbital, corresponding  to  the  emergence  of  the  nerve  from  its  bony 
canal;  (2)  the  maJar,  on  the  most  prominent  part  of  the  malar  bone; 
(3)  an  indeterminate  focus  somewhere  in  the  line  of  the  gum  of  the 
upper  jaw ;  (4)  the  superior  labial,  also  indeterminate ;  (5)  the  palatine, 
rare,  but  occasionally  the  seat  of  intolerable  pain. 

c.  Inframaxillary  Neuralgia. 

When  all  the  branches  of  the  third  division  of  the  fifth  nerve  are 
affected  the  pain  is  localized  in  the  region  of  the  lower  jaw  and  lower 
roAv  of  teeth  (inferior  dental  nerve),  in  the  chin  (mental  branch),  in  the 
tongue  and  mucous  membrane  of  the  mouth  (lingual  nerve),  in  the  cheek 
(buccal  nerve),  and  in  the  temporal  region,  anterior  part  of  the  auricle 
of  the  ear,  and  external  auditory  meatus  (auriculo-temporal  nerve). 

The  painful  points  are:  (1)  The  temporal,  a  little  in  front  of  the 
ear;  (2)  the  inferior  dental,  opposite  the  point  of  emergence  of  that 
nerve;  (3)  the  lingual,  on  the  side  of  the  tongue;  (4)  the  inferior 
labial.     The  parietal   point,    a    little    above    the   parietal    eminence, 


250 


DISOEDEES    OF    MIXED    XEEVES. 


corresponds  to  the  inosculation  of  various  branches  of  the  nerve,  and 
may  occur  in  all  forms  of  trigeminal  neuralgia. 


Fig.  79. 


DlAGK.VM   OF  THE   THIRD    (INFERIOR  JIaXILLARV)    DiVI.SION   OF  THE   FiFTH    NeRVE,    ITS    CONNECTIONS   .*ND 

Chief  Branches.    fFiom  Hermann's  "  Pliysiologj-.") 


V,  Fifth  nerve.     (;,  Its  largest  S(?nsory  root,  with  Ciisserian  ganglion. 

a,  Its  smaller  motor  root  joining  e,  the  thiril  division  of  the  Casserian  ganglion,  to  fi>nii  the  inferior 
maxillary  nerve. 

A,  Anterior  division  of  inferior  maxillary  nerve  (mainly  motor)  supplying  branches  to  the  muscles 

of  mastication,  and  a  terminal  hnccnl  liranch  to  the  mucous  membrane  of  the  mouth. 

B,  Posterior  division  (mainly  sensory)  ;  its  branches  are  marked  — 

1,  Lingual  nerve  ;  1',  Branches  to  the  tongue. 

2,  Inferior  dental  nerve  ;  2'  Its  twigs  to  the  teeth  ;  2",  Incisor  branch ;  2'",  Mental  branch. 

3,  IVIylohyoid  branch  to  digastric  and  mylohyoid. 

4,  Auriculo-temporal  nerve. 

F,  Facial  nerve,     ct,  Its  chorda  ti/mp^ini  branch,  joining  the  lingual  and  running  to  the  submaxillary  gan- 
glion SG,  of  which  it  forms  the  motor  root. 
OG,  Otic  ganglion  : 

ssp,  Ismail  superficial  petrosal  nerve,  connecting  otU:  ginglion  and  facial  nerve. 
M,  Middle  meningeal  artery,  from  the  plexus  upon  which  sympathetic  filaments  pa.ss  to  the  oUc  ganglion 
esp,  External  superficial  petrosal  nev\e,  connecting  the  plexus  on  the  middle  meningeal  artery  with 

the  facial  nerve ; 
gsp.   Great  superficial  petrosal  nerve,  connecting  the  facial  with  Meckel's  ganglion. 

FA,  Facial  artery,  from  the  plexus  upon  which  sympathetic  filaments  pass  to  the  submaxillary 

ganglion. 
FO,  Foramen  ovale.  MF,  ilental  foramen 

SG,  Submaxillary  ganglion 


XEURALGIA    OF   IXDIVIDUAL   XEEVES   AXD   PLEXUSES.      251 

d.  Epileptiform  Neuralgia. 
In   this  form  of  facial   neuralgia  lightning-like  pains  of  the  most 
violent  nature  succeed  each  other  with  the  gi-eatest  rapidity  for  a  few- 
seconds  or  minutes,  and  then  suddenly  vanish.     These  short  attacks 


Fig.  80. 


Fig.  81. 


Figs.  80  and  81.— Cutaneous  Xerves  of  the  Trunk,  Upper  E.xtremitv.     (After  Flower.) 
Sa,  Supraclavicular  nerve. 
IID,  Second  dorsal. 

PS,  Posterior  branches  of  the  spinal  nerves. 
LI,  Lateral  branches  of  the  intercostal  nerves 
AI,  Anterior  branches  of  the  intercostal  nerves. 
II,  Iliac  branch  of  ilio-ingiiinal  nerve. 
I'H',  Ilio-hypogastric  nerve. 
C,  Circumflex  nerve. 
IH,  Intercostal  humeral 
AV.  Xerve  of  Wrisberg 

I'CB,  Internal  cutaneous  branch  of  musculo-spiral  nerve. 
ECB,  External  cutaneous  branch  of  musculo-spiral  nerve. 
ICB,  Internal  cutaneous  nerve. 
MC,  Musculo-cutaueous  nerve. 
K,  Kadial  nerve. 
U,  Ulnar  nerve 
M,  Median  nerve. 


252  DISORDEES    OF    MIXED    NERVES. 

may,  however,  recur  and  follow  each  other  in  quick  succession  for  a 
period  of  hours,  days,  or  even  weeks,  when  a  respite  follows,  and  the 
paroxysm  disappears  for  days,  weeks,  or  even  years,  although  relapses 
are  sure  to  recur  after  a  longer  or  shorter  time.  This  form  of  neural- 
gia is  of  centric  origin,  and  occurs  in  families  with  a  strongly  marked 
neuropathic  tendency,  while  it  is  often  accompanied  by  epilepsy. 

2.  Cervico-occipital  Neuralgia. 

Etiology. — Cervico-occipital  neuralgia  is  usually  excited  by  exposure 
to  cold,  and  occasionally  results  from  disease  of  the  upper  cervical 
vertebne. 

Symptoms. — The  area  of  distribution  of  the  great  occipital  nerve 
(Fig.  77,  GO)  is  the  region  usually  affected,  but  the  pain  may  radiate 
widely  into  the  area  of  distribution  of  the  other  branches  of  the  cervical 
plexus,  and  even  over  the  brows,  temples,  cheeks,  or  lower  part  of  the 
ftice,  so  that  the  affection  may  be  mistaken  for  trigeminal  neuralgia. 
The  most  usual  concomitant  symptoms  are  hyperf^sthesia  or  an;v?stliesia 
of  the  occipital  region,  spasm  of  the  cervical  muscles,  and  considerable 
irritation  and  swelling  of  the  cervical  glands. 

The  painful  points  are :  (1)  the  occipital  point,  about  midway  be- 
tween the  mastoid  process  and  the  spinous  processes  of  the  upper  cer- 
vical vertebra;  (2)  the  parietal  point,  over  the  parietal  eminence. 
The  track  of  the  nerve  over  the  occiput  is  often  painful,  and  the 
spinous  processes  of  the  upper  cervical  vertebra  are  generally  tender 
on  pressure. 

o.  Phrenic  Neuralgia. 

It  is  believed  by  Peter  that  the  phrenic  is  a  mixed  instead  of  being  a 
purely  motor  nerve.  The  symptoms  of  phrenic  neuralgia,  as  described 
by  this  author,  are  severe  pains  at  the  point  where  the  nerve  descends 
over  the  scalenus  anticus  muscle  in  its  course  through  the  chest,  at 
the  anterior  and  lower  part  of  the  thorax,  and  along  the  line  of  attach- 
ment of  the  diaphragm.  Pain  in  the  shoulder  is  a  constant  and  charac- 
teristic symptom.  Phrenic  neuralgia  is  usually  a  symptom  of  epilepsy, 
hysteria,  and  angina  pectoris,  and  is  met  with  occas'^ionally  as  a  sei)arate 
affection. 

The  painful  points  are:  (1)  The  spinous  processes  of  the  upper 
cervical  vertebrae;  (2)  the  phrenic  nerve  in  its  course  along  the  sub- 
clavicular fossa  ;  (3)  the  line  of  attachment  of  the  diaphragm,  especially 
anteriorly  between  the  seventh  and  tenth  ribs ;  (4)  a  point  over  the 
cartilage  of  the  third  rib. 


NEURALGIA   OF  INDIVIDUAL  NERVES  AND  PLEXUSES.      253 

4.  Cekvico-brachial  Xeiraloia. 

Etiology. — The  most  important  exciting  causes  are  the  various  in- 
juries to  which  the  upper  extremities  are  so  peculiarly  exposed.  It 
may  also  be  caused  by  lead-poisoning  and  malaria,  and  may  be  a 
symptom  of  central  diseases,  as  tabes  hemiplegia  and  proc^ressive  mus- 
cular atrophy. 

Si/rnptoms. — Cervico-brachial  neuralgia  occurs  in  the  area  of  distri- 
l)Ution  of  the  sensory  branches  of  the  brachial  plexus  (Figs.  80  and  81) 
and  the  posterior  branches  of  the  four  lower  cervical  nerves.  The  pain 
is  more  or  less  continuous,  and  is  of  a  dull,  boring,  or  burnino-  char- 
acter, interrupted  by  paroxysms  of  lancinating  pains,  which  shoot 
through  the  arm  along  the  course  of  the  nerves.  It  often  occurs  in 
nocturnal  paroxysms  which  last  through  the  night  and  may  disap])ear 
during  the  day.  The  pain  may  have  its  seat  in  the  upper  arm  or  fore- 
arm, or  may  extend  into  the  hand  and  fingers,  but  it  is  generallv 
widely  distrifented,  and  the  intimate  interweaving  of  the  various  nerve 
trunks  in  the  plexus  renders  it  difficult  to  determine  what  nerve  roots 
or  l)ranches  of  the  plexus  are  implicated.  When  the  pain  is  situated 
near  the  periphery  it  may  be  limited  to  one  branch  of  a  nerve.  The 
violent  burning  pain  described  by  S.  Weir  Mitchell  under  the  name  of 
'"causalgia"  is  often  present  in  the  neuralgiie  which  result  from  gun- 
shot injuries  of  the  nerves. 

The  pcmiful  points,  which  are  somewhat  indefinite,  are:  (1)  an 
axillafy  pointy  corresponding  to  the  brachial  plexus;  (2)  ^  scap)ular 
^^o/n^,  corresponding  to  the  lower  angle  of  the  scapula;  (3)  a  shoulder 
point,  corresponding  to  the  emergence  through  the  deltoid  of  the 
cutaneous  branches  of  the  circumflex;  (4)  a  mrdian  cephalir  jjoint,  at 
the  bend  of  the  elbow ;  (5)  an  external  humeral  point  about  three 
inches  above  the  elbow;  (6)  a  superior  ulnar  point,  over  the  ulnar 
nerve  in  its  course  between  the  olecranon  and  the  epitrochlear ;  and 
(7)  a  radial  point,  where  the  nerve  becomes  superficial  at  the  lower  and 
external  aspect  of  the  forearm.  Painful  points  may  occasionally  be 
developed  by  the  side  of  the  lower  cervical  vertebrtie,  corresponding  to 
the  posterior  branches  of  the  lower  cervical  nerves. 

The  concomitant  symptoms  consist  of  cutaneous  hypersesthesia,  numb- 
ness, and  formication,  or  a  considerable  degree  of  ana?sthesia.  Radiat- 
ing pains  are  felt  in  the  region  of  distribution  of  the  cervical  plexus, 
and  of  the  upper  dorsal  and  intercostal  nerves. 

The  motor  disorders  consist  of  twitchings  of  the  muscles  of  the 
upper  extremities,  and  in  aggravated  cases  they  may  be  maintained  m 


2o4  DISOEDEES    OF    MIXED    NEEVES. 

:i  State  of  persistent  spasm.  In  chronic  cases  some  of  the  muscles  may 
he  enfeebled  or  completely  paralyzed,  but  neuritis  is  then  probaldy 
present. 

The  vaso-motor  disorders  are  coldness  and  pallor,  or  redness  and 
heat  of  the  affected  extremity. 

The  trophic  disorders  consist  of  eruptions  of  herpes,  Ijut  the  aggra- 
vated cases  which  are  caused  by  gunshot  and  other  injuries  of  the 
nerves  are  complicated  by  pemphigus,  obstinate  ulcers,  glossy  skin, 
and  changes  in  the  groAvth  of  the  nails  and  hair. 

5.    DORSO-INTERCOSTAL    NeURAL(;IA. 

Etiology. — Women  are  especially  liable  to  this  form  of  neuralgia. 
It  comes  on  usually  between  the  ages  of  twenty  and  forty  years,  in 
nervous,  hysterical,  and  anemic  subjects,  and  its  usual  exciting  causes 
are  oversuckling,  menorrhagia,  and  leucorrhoea. 

The  exciting  causes  of  dorso-intercostal  neuralgia  are  exposure  to 
cold,  injuries  of  various  kinds,  neuritis,  neuromata,  disease  of  the  ver- 
tebnie  or  ribs,  aortic  aneurisms,  pulmonary  phthisis,  dilatation  of  the 
venous  plexus  in  the  interior  of  the  vertebral  canal,  and  diseases  of 
the  spinal  cord,  such  as  transverse  myelitis,  spinal  meningitis,  spinal 
and  meningeal  tumors,  and  locomotor  ataxia. 

Symptoms. — The  pain  of  intercostal  neuralgia  is  seated  in  the  area 
of  distribution  of  the  sensory  branches  of  the  twelve  pairs  of  dorsal 
nerves;  it  is  of  a  dull,  and  tensive  character,  and  is  usually  continuous, 
but  it  is  occasionally  interrupted  by  tearing,  lancinating,  or  burning 
pains.  The  pain  is  aggravated  by  all  violent  respiratory  movements, 
and  by  slight  pressure  on  the  skin,  but  it  is  often  relieved  by  firm  and 
steady  pressure.  The  pain  not  infrequently  radiates  tOAvards  the  back 
and  arm,  or  into  the  loins  or  lower  extremities,  and  this  form  of 
neuralgia  may  be  associated  with  brachial  and  lumbo-abdominal  neural- 
gia, or  with  angina  pectoris.  The  seat  of  true  intercostal  neuralgia  is 
the  skin  of  the  anterior  and  lateral  wall  of  the  thorax  and  abdomen  as 
far  down  as  the  symphysis  pubis,  and  when  the  first  two  nerves  are 
attacked  the  pain  extends  to  the  axilla  and  inner  surface  of  the  arm. 
When  the  posterior  branches  are  affected  the  pain  is  seated  in  the  back 
an<l  loins  as  fiir  down  as  the  crista  ilii.  Dorso-intercostal  neuralgia  is 
generally  unilateral  except  when  it  is  a  symptom  of  spinal  disease,  and 
the  area  of  distribution  of  one  or  two  branches  on  the  left  side  from 
the  fifth  to  the  ninth  nerve  is  the  part  most  usually  affected. 

The  concomitant  symptoms  consist  of  hypersesthesia  of  the  affected 
skin,  while  a  circumscribed  patch  of  antesthesia  has  occasionally  been 


XEURALCxIA    OF   INDIVIDUAL   NERVES   AND   PLEXUSES.      255 


Ulg 


met  Avith.  Spasm  of  the  intercostal  muscles,  givinf  rise  to  catclii 
breathing  like  that  of  pleurisy,  is  often  present.  Of  the  vaso-motor 
and  trophic  disorders,  herpes  zoster  is  the  most  common ;  it  may  be 
present  without  neuralgia  in  young  persons,  but  the  neuralgia  precedes 
and  outlasts  the  eruption  in  old  persons. 

The  painful  points  are:  (1)  a  vertebral  point,  close  to  the  vertebral 
column  over  the  point  of  emergence  of  the  nerve  from  the  intercostal 
foramen ;  (2)  a  lateral  point,  over  the  spot  in  which  the  lateral  per- 
forating branch  becomes  subcutaneous ;  and  (3)  an  ajiterior  or  sternal 
point,  over  the  spot  where  the  anterior  perforating  branch  pierces  the 
muscle  close  to  the  sternum,  and  in  the  abdomen  over  the  rectus  muscle. 
The  whole  length  of  tlie  intercostal  nerves  is  often  sensitive,  and 
several  of  the  spinous  processes  of  the  corresponding  vertebra  tender  to 
pressure. 

Mastodynia. 

Etiology. — Neuralgia  of  the  female  breast  forms  a  special  variety  of 
intercostal  neuralgia.  It  may  appear  at  puberty  in  persons  having  a 
strong  neurotic  tendency,  while  aniiemia,  chlorosis,  and  hysteria  act 
as  predisposing  causes.  It  is  also  liable  to  come  on  during  pregnancy, 
although  a  large  proportion  of  the  pains  felt  in  the  gland  during  this 
period  are  caused  by  mechanical  distention.  The  exciting  causes  of 
mastodynia  are  irritation  of  cracked  nipples,  shrinking  of  the  nipples 
during  lactation,  injuries  of  the  gland,  and  neuromata  and  painful 
tubercles  of  the  nerves. 

Symptoms. — The  pain  of  "irritable  breast"  is  very  violent;  it  is 
described  as  tearing,  cutting,  boring,  and  lancinating,  and  appears  in 
paroxysms  which  are  usually  of  short  duration,  but  may  last  several 
hours.  The  breast  feels  heavy,  and  the  patient  cannot  lie  on  the 
affected  side,  while  the  slightest  contact,  even  the  pressure  of  the 
clothes,  is  unbearable.  There  is  generally  a  great  deal  of  hyperfesthesia, 
and  the  paroxysms  are  sometimes  accompanied  by  vomiting.  The  pain 
radiates  into  adjoining  regions,  and  the  severity  of  the  paroxysm  is 
increased  during  the  catamenial  ])eriod. 

Painful  points  may  be  found  on  the  nipple  or  on  the  sides  of  the 
breast,  but  they  are  indefinite.  The  spinous  processes  of  the  second 
to  the  sixth  dorsal  vertebra  are  generally  tender  to  pressure. 

6.  Lumbar  Neuralgia. 

Etiology. — The  special  exciting  causes  of  lumbar  neuralgia  are  com- 
pression of  the  nerves  by  hernia,  accumulation  of  feces,  cancer  in  the 
pelvis  or  in  the  vertebral  column,  diseases  of  the  uterus  and  vagina. 


256  DISOEDERS    OF    MIXED    NERVES. 

coitus,  ])Soas  abscess,  chronic  spinal  diseases,  and  diseases  of  tlie  ver- 
tebral column. 

Symptoms. — Lumbar  neuralgia  includes  all  forms  having  their  seat 
in  the  area  of  distribution  of  the  sensory  branches  of  the  first  four 
pairs  of  lumbar  nerves.  The  pain  is  usually  limited  to  one  or  two  of 
the  branches  of  the  plexus.  Lumbar  neuralgia  may  be  divided  into 
(1)  lunibo-abdominal  and  (2)  femoral  neuralgia,  while  it  will  be  conve- 
nient to  describe  in  this  place  (3)  neuralgia  of  the  external  generative 
organs,  even  although  these  organs  and  the  neighboring  parts  are  sup- 
phed  by  branches  from  the  sacral  as  well  as  from  the  lumbar  nerves. 

a.   Luinho-nhdominal  Neuraliiia. 

The  \n\m  in  this  variety  is  seated  in  the  loins,  hypogastrium,  mons 
venei-is,  and  scrotum  or  labia  majora,  and  extends  over  the  crista  ilii  as 
far  as  the  buttock,  while  the  inguinal  region  may  bo  occasionally 
affected.  The  usual  concomitant  symptoms  are  spasm  of  the  cremaster, 
vomiting,  herpes,  and  increased  sexual  desire  with  priapism  and  ejacu- 
lation of  seminal  fluid. 

The  painful  points  are:  (1)  Vertebral  points,  corresponding  to  the 
posterior  branches  of  the  respective  nerves ;  (2)  an  iliac  point,  at  the 
middle  of  the  crista  ilii ;  (3)  an  ahdo in inal point,  at  the  side  of  the  linea 
alba  above  the  symphysis  pubis;  (4)  an  inguinal  point,  in  the  groin 
near  the  exit  of  the  spermatic  cord ;  (5)  a  scrotal  or  labial  point,  in 
the  scrotum  or  labium  majus.  The  pain  frequently  radiates  into 
neio-hborino;  nerve  territories. 

b.  Femoral  Neuralgia. 

(j)  Neuralgia  of  the  lateral  cutaneouff  nerve  of  the  tliigh  is  situated 
in  the  outer  and  part  of  the  posterior  aspect  of  the  thigh  as  far  as  the 
knee. 

The  painful  points  are:  (1)  Spot  over  anterior  superior  spinous 
process,  which  is  constant;  (2)  spots  along  the  outer  aspect  of  the 
thigh,  which  are  less  constant. 

(jj)  Crural  neuralgia  is  situated  in  the  middle  and  inner  part  of  the 
anterior  surface  of  the  thigh,  the  anterior  surface  of  the  knee,  and 
the  inner  surface  of  the  leg,  and  of  the  foot  as  far  as  the  great  toe. 
Tlie  concomitant  symptoms  are  hyperiesthesia  or  anesthesia  of  the  skin, 
especially  in  the  vicinity  of  the  knee-joint,  a  feeling  of  numbness  or 
formication  in  the  region  of  distribution  of  the  saphenous  nerve,  and  a 
feeling  of  weariness  on  exertion,  or  paresis  of  the  muscles  of  the  thigh. 


NEURALGIA   OF   INDIVIDUAL   NERVES   AND   PLEXUSES.      257 

The  painful  points  are:  (1)  One  in  the  fold  of  the  groin,  where  the 
nerve  emerges  from  the  pelvis ;  (2)  one  at  the  inner  side  of  the  patella, 
Avhere  the  saphenous  nerve  becomes  subcutaneous;  (3)  one  in  front  of 
the  ankle-joint;  and  (4)  one  at  the  base  of  the  great  toe. 

(jjj)  Obturator  neuralgia  is  situated  in  the  inner  side  of  the  thio-h, 
and  extends  as  far  as  the  knee-joint.  It  is  associated  with  obturator 
hernia,  and  the  concomitant  symptoms  are  formication  on  the  inner 
surface  of  the  thigh,  and  a  feeling  of  stiffness  and  immobility  of  the 
adductors  of  the  thigh. 

c.  Neuralgia  of  the  External  Organs  of  Greneration. 

(j)  Neuralgia  of  the  Penis  or  Clitoris. — The  pain  has  its  seat  in  the 
glans  and  extends  to  the  root  of  the  penis.  The  pain  is  violent,  lan- 
cinating, and  burning,  and  may  be  unilateral  or  bilateral ;  it  is  in- 
creased by  sexual  intercourse  and  urination,  and  it  may  be  accompanied 
by  priapism  and  frequent  ejaculations.  The  clitoris  is  sometimes  the 
seat  of  ])ainful  erections  in  the  early  stage  of  tabes  dorsalis. 

(jj)  Neuralgia  scrotalis  vel  labialis  is  a  common  symptom  of  lumbo- 
abdominal  neuralgia.  The  scrotum  or  lal)ium  majus  is  often  tender  to 
touch. 

7.    NEUIlAL(iIA    OF    THE    SaCRAL    AND    COCCYGEAL    NeRYES. 

Neuralgia  affecting  the  sensory  branches  of  the  sacral  and  coccygeal 
nerves  may  be  divided  into  (a)  sciatica,  (b)  plantar  neuralgia,  and  (c) 
coccygodynia. 

a.  Neuralgia  Ischiadica  {Sciatica). 

Etiology. — Heredity  does  not  appear  to  exercise  much  influence  in 
the  production  of  sciatica.  The  largest  number  of  cases  occur  between 
forty  and  fifty  years  of  age  or  during  the  period  of  commencing  bodily 
degeneration,  and  after  the  age  of  thirty  years  males  are  much  more 
frequently  attacked  than  females.  The  exciting  causes  are  exposure 
to  cold,  gunshot  wounds,  and  injuries  of  the  nerve  by  blows,  fixlls  on 
the  buttock,  or  by  compression  of  the  nerve  in  difficult  labors,  especially 
wdien  the  forceps  is  used.  Other  causes  are  mechanical  pressure  on  the 
nerve  from  sitting  on  hard  seats,  enlargements  and  displacements  of 
the  uterus,  pregnancy,  accumulation  of  feces  in  the  sigmoid  flexure, 
and  pelvic  tumors.  Portal  congestion,  habitual  constipation,  and  all 
conditions  which  g-ive  rise  to  congestion  of  the  hemorrhoidal  and  other 
pelvic  veins  may  cause  sciatica,  while  it  may  also  result  from  the  poisons 
of  rheumatism,  gout,  and  syphilis. 

17 


258  DISORDERS    OF    MIXED    NERVES. 

Symptoms. — The  pain  is  seated  in  the  area  of  distribution  of  the  sen- 
sory branches  of  the  small  and  great  sciatic  nerves  (Fig.  82).  An 
attack  of  sciatica  is  generally  preceded  by  premonitory  symptoms,  such 
as  a  sensation  of  fluid  trickling  over  the  skin,  or  a  feeling  of  cold  or 
heat,  formication,  and  a  sense  of  stiifness  and  dragging.  The  symptoms 
of  true  neuralgia  now  make  their  appearance,  and  consist  of  lightning- 
like pains  which  increase  in  intensity  and  recur  with  greater  and 
o-reater  frequency,  until  a  violent  paroxysm  of  almost  continuous  pain 
is  established.  After  a  time  the  violence  of  the  pain  abates  and  the 
patient  has  an  interval  in  which  he  is  comparatively  but  not  completely 
free  from  pain,  but  after  a  longer  or  shorter  period  he  is  seized  with 
another  violent  paroxysm.  The  pain  is  usually  superficial,  but  at  times 
it  may  be  felt  in  and  between  the  muscles,  or  even  in  the  bones ;  it 
proceeds  from  one  or  more  fixed  points,  and  generally  shoots  along  the 
branches  of  the  nerve  to  the  periphery,  while  a  nocturnal  exacerbation 
is  frequently  experienced.  It  is  aggravated  by  all  movements  of  the 
limb,  and  such  actions  as  coughing,  sneezing,  straining  at  stool,  or 
even  simple  contact  of  the  bedclothes  may  bring  on  a  paroxysm,  and 
consequently  the  limb  is  maintained  in  a  fixed  position  with  all  the 
joints  slightly  flexed. 

The  pain  is  most  commonly  felt  in  the  posterior  surface  of  the  thigh, 
commencing  in  the  neighborhood  of  the  sciatic  foramen,  and  extending 
to  the  popliteal  space  and  calf  of  the  leg.  The  next  part  most  fre- 
quently aftected  is  the  peroneal  region,  including  the  anterior  and 
external  surface  of  the  leg  and  the  dorsum  of  the  foot.  Sometimes 
the  whole  area  of  distribution  of  the  sciatic  nerves  is  affected,  and  the 
violence  of  the  pain  may  shift  from  one  region  to  another.  Violent 
pains  are  also  felt  in  the  sacrum  and  loins  from  implication  of  the  pos- 
terior branches  of  the  sacral  nerves,  while  the  pain  may  also  shoot  into 
the  lumbar  nerves  and  their  branches,  into  the  sciatic  nerve  of  the 
opposite  side,  or  into  more  remote  nerve  territories. 

The  concomitant  symptoms  are  hypen\?sthesia,  or  partial  anaesthesia, 
and  diminution  of  the  electric  sensibility  of  portions  of  the  skin, 
cramps  of  particular  groups  of  muscles,  which  are  especially  severe  at 
night  when  the  patient  is  falling  asleep,  and  in  long-standing  cases 
considerable  diminution  of  motor  power,  which  renders  the  gait  limp- 
ing. Complete  paralysis  only  occurs  when  there  is  neuritis.  The 
most  usual  vaso-motor  and  trophic  disorders  are  pallor  and  coldness, 
or  redness  and  heat  of  the  surface,  increased  secretion  of  sweat,  wast- 
ing or  occasionally  hypertrophy  of  some  of  the  muscles. 

The  painful  points  are :  (1)  a  series  of  points  reaching  from  the 
lower  end  of  the  sacrum  up  to  the  crista  ilii,  representing  the  posterior 


NEUEALGIA   O  P^   INDIVIDUAL  NERVES  AND  PLEXUSES.      259 

Fig.  82. 


CUTANEC<JS   XERVES   OF  THE   LoWER    EXTREMITY.      (After  FlOWER. 

Lumbar  Plexus. 

IH,  Ilio-hypogastric  nerve. 

II,  Ilio-inguinal. 

IIL,  Second  lumbar  nerve. 

GC,  Genito-crural. 

EC,  External  cutaneous. 

MC,  Middle  cutaneous. 

IC,  Internal  cutaneous^ 

IS,  Internal  saphenous. 

PP,  Plexus  patellw.  ^ 

Sacral  Plexus.  ^^ 

DP,  Dorsalis  penis  of  pudiifr. 

IP,  Inferior  hemorrhoidal  of  pudic. 

P,  Superficial  perineal  of  pudic  and  inferior  pudendal  of  small  sciatic. 

IG,  Inferior  gluteal  of  small  sciatic. 

SS,  Small  sciatic.  ' 

EP,  Branches  from  external  popliteal.       * 

ES,  External  saphenous. 

5It'S,  Musculo-cutaneous. 

AT,  Branches  of  anterior  tit^al. 

PT,  Branch  of  posterior  tibial. 


/^ 


260  DISORDERS    OF    MIXED    NERVES. 

branches ;  (2)  a  point  opposite  the  emergence  of  the  great  and  small  sciatic 
nerves  from  the  pelvis ;  (3)  a  point  opposite  the  spots  where  the  ascend- 
ino-  branches  of  the  small  sciatic  become  subcutaneous ;  (4)  several  points 
at'the  posterior  aspect  of  the  thigh  corresponding  to  the  emergence  of  the 
cutaneous  nerves;  (5)  -a  fibular  point  at  the  head  of  the  fibula;  (6)  an  ex- 
ternal maUeolar  point  behind  the  ankle ;  (7)  an  internal  malleolar  point. 
The  sacral  plexus  is  frequently  tender  on  pressure  when  examined 
through  the  anus  or  vagina. 

h.  Neuralgia  Flantaris  {Erythemomegalalgia). 

The  first  accurate  account  of  this  aft'ection  was  given  by  Dr.  S. 
Weir  Mitchell,  under  the  title  of  ''  A  rare  vaso-motor  neurosis  of 
the  extremities,"  or  "Erythemomegalalgia,"  but  inasmuch  as  the  vaso- 
motor disorders  are  preceded  and  accompanied  by  severe  paroxysms  of 
pain,  I  see  no  reason  why  the  affection  should  not  be  regarded  as 
plantar  neuralgia,  or  as  a  neuritis  of  the  plantar  nerves. 

Etiology. — This  disease  occurs  nearly  always  in  the  male  sex,  and 
comes  on  after  some  constitutional  disease  as  a  low  fever,  after  pro- 
lono-ed  exertion,  or  as  a  sequel  of  an  attack  of  gonorrheal  rheu- 
matism. It  is,  indeed,  probable  that  the  cases  of  obstinate  pain  in 
the  sole  of  the  foot,  described  by  Dr.  EUiotson  as  folloAving  gonorrhoeal 
rheumatism,  belong  to  this  category. 

Symptoms. — The  pain  usually  begins  in  the  ball  of  the  great  toe,  or 
in  the  heel,  and  often  extends  over  a  great  part  of  the  sole,  and  may 
reach  the  dorsum  of  the  foot,  and  the  leg.  It  is  felt  at  first  towards 
night,  and  is  relieved  by  the  night's  rest,  while  it  is  increased  by  walk- 
ing, the  erect  posture,  or  even  by  allowing  the  foot  to  hang  down. 
The  pain  in  the  early  stage  of  the  disease  consists  of  a  deep-seated 
aching,  but  after  a  time  it  becomes  of  a  burning  character,  and  is  then 
aggravated  by  warmth  and  relieved  by  cold  and  the  recumbent  posture. 
The  most  characteristic  symptom  of  the  affection,  however,  is  a  flushing 
of  the  painful  area,  which  comes  on  with  exertion  or  when  the  feet  are 
allowed  to  hang  down,  and  is  accompanied  by  swollen  veins  and  violent 
throbbing  of  the  arteries.  The  shaded  part  in  the  annexed  diagram 
shows  distribution  of  the  reddened  surface  in  one  of  Dr.  Mitchell's 
cases.  In  the  worst  cases  the  extremity  is  pale  and  cold  when  the 
patient  is  at  rest.  In  aggravated  cases  the  pain  is  so  severe  as  to 
render  walking  all  but  impossible,  and  when  persisted  in  intense  redness 
and  swelling  are  occasioned,  the  patient  sleeps  with  his  feet  uncovered, 
and  may  even  be  reduced  to  crawl  on  his  hands  and  knees,  or  is  obliged 
to  be  carried  about  in  order  to  avoid  placing  his  feet  on  the  ground. 


XEL'RALGIA  OF   INDIVIDUAL  NERVES  AND   PLEXUSES.      261 

The  feet  are  generally  bathed  in  sour-smelling  sweat,  and  the  skin  of 
the  sole  mav  have  a  sodden  appearance,  becoming  somewhat  glazed 
during  the  paroxysm  of  pain  and  redness.  The  disease  is  sometimes 
progressive,  and  in  its  later  stages  may  be  associated  with  evidences  of 
spinal  disease,  such  as  girdle  pains  and  partial  paralysis  with  atrophy 
of  some  of  the  muscles  of  the  leg,  while  the  fliradic  contractility  has 
been  found  diminished  in  the  muscles  of  the  limb  most  affected.     The 

Fig.  83. 


disease  is  generally  bilateral,  and  in  one  case  observed  by  Dr.  Mitchell 
the  hands  were  attacked  as  well  as  the  feet.  In  each  of  several  cases 
which  came  under  my  observation  a  tender  spot  was  present  in  the 
centre  of  the  heel,  the  whole  course  of  the  external  plantar  nerve  was 
tender  to  pressure,  and  painful  points  were  found  between  the  heads  of 
the  metatarsal  bones,  over  the  bifurcation  of  the  brandies  of  the  plantar 
nerves  for  the  digits. 

c.  Neuralgia  of  the  Coccygeal  Nerves  [Qoccygodynia). 

Etiology. — This  affection  occurs  generally  in  women  in  consequence 
of  injury  to  the  coccyx  fi'om  a  fall,  or  during  labor.  It  may  also  be 
caused  by  exposure  to  cold,  or  may  originate  spontaneously. 

Symptoms. — The  chief  symptom  of  coccygodynia  consists  of  pain 
in  the  region  of  the  coccyx  when  the  patient  sits  or  walks,  and  it  is 
often  felt  during  micturition  and  defecation,  especially  if  there  be  much 
straining.     Pressure  on  the  coccyx,  by  the  finger,  aggravates  tliis  pain. 


262  DISORDEES    OF    MIXED    NERVES. 

Diagnosis.— Scintkai  may  be  mistaken  for  myalgia  of  the  thigh  or 
leo-,  but  the  pain  in  myalgia  has  a  diffused  localization,  so  that  the 
patient  indicates  its  seat  with  his  Avhole  hand,  whilst  in  neuralgia  he 
points  to  it  Avith  his  finger.  Sciatica  may  also  be  mistaken  for  chronic 
hip-joint  disease  or  hysterical  coxalgia,  but  an  error  will  be  avoided  by 
a  careful  observation  of  the  movements  of  the  joint,  of  the  presence  or 
absence  of  pain  Avhen  the  head  of  the  femur  is  pressed  against  the  ace- 
tabulum, or  of  painful  points,  and  the  concomitant  symptoms  of  neuralgia. 
A  valuable  diagnostic  sign  of  sciatica  is  afforded  by  passively  flexing 
the  affected  extremity  at  the  hip-joint,  whilst  the  leg  is  extended  on  the 
thigh  which  is  affected,  when  the  patient  is  lying  on  his  back,  by  grasp- 
ino-  the  heel  and  raisino;  it  from  the  bed.  This  movement  causes  the 
nerve  to  be  stretched  over  the  trochanter,  and  to  be  likewise  pressed 
upon  by  the  tense  muscles,  and  the  consequent  irritation  of  the  nerve 
induces  a  reflex  spasm  of  all  the  muscles,  Avhich  renders  the  limb  as 
rigid  as  a  bar  of  iron,  and  arrests  the  movement  when  the  heel  is 
raised  about  a  foot  from  the  bed.  If  the  patient  is  standing,  essentially 
the  same  test  may  be  applied  by  asking  him  to  bend  down  and  touch 
the  toe  of  the  affected  limb  with  the  tips  of  the  fingers  of  the  corre- 
sponding hand,  while  keeping  the  legs  extended  at  the  knees.  The 
nerve  is  thus  put  upon  the  stretch  and  the  movement  is  arrested  long 
before  the  fingers  reach  the  toe. 

Plantar  neuralgia  is  most  liable  to  be  mistaken  for  an  affection 
described  by  Gross,  which  is  peculiar  to  tailors,  and  named  ])odyni(i. 
It  appears  to  depend  upon  subacute  inflammation  of  the  periosteum, 
and  consists  of  a  burning  pain  in  some  part  of  the  sole,  but  there  is 
no  redness.  A  painful  spot  on  the  heel  may  be  observed  after  syphilis, 
but  careful  examination  will  reveal  a  node  on  the  os  calcis. 

8.  Visceral  Neuralgia. 

The  various  plexuses  of  the  lymphatic  system  are  liable  to  be 
afi"ected  by  severe  attacks  of  neuralgia. 

a.  Neuralgia  of  the  Pharyngeal  and  (Esophageal  Plexuses. 

Neuralgia  of  the  pharynx  and  soft  palate  occurs  in  young  girls,  and 
occasionally  in  married  women  between  thirty  and  forty  years  of  age. 
Patients  complain  of  pain  in  the  soft  palate,  which  is  generally  limited 
to  one  side. 


XEURALGIA   OF   INDIVIDUAL  XERVES  AND   PLEXUSES.      263 

b.  Neuralgia  Mesenteriea  {Colic,  Unteralgia,  Colica  Saturnina). 

Etiology. — The  causes  of  colic  are  local  irritation  of  the  mucous 
membrane,  such  as  is  produced  by  the  presence  of  worms  or  undigested 
food  in  the  intestines,  by  increased  irritability  of  the  nerves,  occa- 
sioned by  disease  of  the  intestines,  by  indirect  irritation  from  disease  of 
the  uterus,  ovaries,  or  remote  organs ;  spinal  diseases,  like  tabes  dor- 
salis,  central  affections  like  hysteria,  and  poisons  circulating  in  the 
blood,  like  the  poison  of  gout  and  rheumatism,  or  mineral  poisons, 
the  chief  of  them  being  lead,  which  produces  the  most  obstinate  and 
severest  form  of  colic. 

Symptoms. — In  colic  the  patient  is  suddenly  attacked  with  severe 
twisting  or  griping  pains  in  the  abdomen,  which  begin  and  are  most 
severe  about  the  umbilical  region,  but  may  spread  over  the  entire  abdo- 
men, and  are  liable  to  change  their  position.  The  pains  occur  in 
paroxysms,  which  are  followed  by  periods  of  remission  or  complete  in- 
termission. The  bowels  are  usually  constipated,  and  distended  with 
flatus,  so  that  a  very  tympanitic  note  is  afforded  on  percussion,  and 
when  the  hand  is  placed  upon  the  abdomen  the  bowels  can  be  felt  roll- 
ing about  with  flatus,  Avhile  the  abdominal  muscles  are  felt  contracted, 
hard,  and  knotty.  Colic  may  occasionally  be  associated  with  diarrhoea. 
In  lead  colic  the  abdomen  is  retracted,  and  there  are  obstinate  constipa- 
tion, nausea,  vomiting,  eructations,  and  hiccough,  while  the  blue  line 
on  the  gums  will  indicate  the  presence  of  the  poison  in  the  system.  In 
colic  uniform  pressure  of  the  abdomen  almost  always  affords  relief,  and 
the  patient  usually  bends  forwards,  or  lies  with  the  face  downwards,  and 
presses  it  with  both  hands.  During  the  attack  the  face  and  extremities 
are  pale  and  cold,  and  the  action  of  the  heart  becomes  slow  and  feeble, 
and  if  the  attack  be  prolonged,  there  may  be  symptoms  of  more  or  less 
complete  collapse,  and  the  patient  feels  faint  and  weak,  and  experiences 
a  sense  of  impending  death  just  as  is  felt  in  angina  pectoris.  The 
action  of  the  heart  is  universally  weak  in  lead  colic,  and  the  pulse, 
although  occasionally  quickened,  is,  as  a  rule,  slow. 

c.  Neuralgia  G-astrica  vel  Coeliaca  {Cardialgia,  Gfastralgia, 
G-astrodynia). 

Etiology. — Gastralgia  is  more  common  in  youth  than  in  old  age  and 
in  women  than  in  men.  It  is  often  associated  with  anaemia  and  chlorosis 
and  is  not  an  unfrequent  manifestation  of  hysteria.  A  very  severe 
form  of  gastralgia,  coming  on  in  spontaneously  recurring  paroxysms, 


264  DISORDEES    OF    MIXED    NERVES. 

named  gastric  crises,  is  a  very  frequent  and  distressing  symptom  ot 

locomotor  ataxia. 

>,SV///^;>fo;»«.— Gastralgia  is  characterized  by  paroxysmal  attacks  of 
pain  in  the  epigastric  region  which  may  radiate  upwards  to  the  back 
between  the  shoulders,  or  to  the  middle  of  the  sternum.  The  attack 
comes  on  suddenly,  without  premonitory  symptom,  and  the  pain,  whicli 
is  very  severe,  generally  intermits  after  a  few  minutes,  but  soon  recurs 
with  greater  intensity,  and  after  repeated  intermissions  and  recurrences 
it  finally  disappears.  Pressure  over  the  cartilages  of  the  false  ribs  on 
the  left  side,  or  on  the  corresponding  intercostal  spaces,  may  cause  pain, 
and  the  spinous  processes  of  some  of  the  dorsal  vertebrae  may  be  tender 
on  pressure.  Tlie  pain  of  gastralgia  is  relieved  by  firm  and  uniform 
pressure,  and  tenderness  of  the  epigastrium  is  generally  absent.  The 
upper  portions  of  the  recti  muscles  are  strongly  contracted  during  the 
attack  and  the  abdominal  walls  are  rendered  tense  and  unyielding,  whilst 
the  epigastric  region  is  usually  retracted.  The  pulse  is  generally  slow 
and  feeble;  the  arterial  tension  is  low;  the  extremities  are  cold  and 
pale  ;  and  towards  the  end  of  the  attack  the  patient  may  suffer  from 
chilliness  and  a  feeling  of  oppression  and  faintness  like  that  of  angina 
pectoris  reflectoria.  The  attack  often  terminates  by  copious  vomiting, 
the  food  contained  in  the  stomach  is  first  ejected,  and  then  large  quanti- 
ties of  watery  fluid  mixed  with  bile  and  blood,  and  in  aggravated  cases, 
mucus;  while  if  the  urine  be  examined  during  or  soon  after  the  attack 
it  is  often  found  to  contain  a  small  (piantity  of  albumen. 

Tabetic  gastric  crisis  is  a  variety  of  gastralgia  which  ])egins  during 
an  attack  of  the  lancinating  pains  of  locomotor  ataxia.  The  jiatient 
complains  of  pain  which  starts  from  the  groins,  and  passes  up  each 
side  of  the  abdomen  to  become  fixed  in  the  epigastrium,  while  at  the 
same  time  severe  lightning  pains  dart  from  between  the  shoulders  and 
radiate  round  the  base  of  the  thorax.  Severe  vomitincr  now  sets  in, 
just  as  occurs  in  all  severe  cases  of  gastralgia.  The  patient  suffers 
during  the  attack  from  a  profound  malaise ;  the  action  of  the  heart  is 
accelerated,  and  the  lightning  pains  are  unusually  severe.  The  attack 
may  last  without  respite  for  two  or  three  days,  and  may  recur  every  two 
or  three  weeks  although  the  usual  interval  betAveen  them  is  not  less  than 
a  month. 

d.  Neuralgia  Hepatica  {Hepatalgia). 

Etiology. — Hepatic  colic  is  usually  the  result  of  the  passage  of  biliary 
calculi  through  the  cystic  and  common  ducts,  but  colic  of  similar  char- 
acter sometimes  occurs  in  neurotic  subjects  in  the  absence  of  any  signs 
of  biliary  obstruction  and  it  is  regarded  as  of  purely  neuralgic  origin. 


NEURALGIA    OF   INDIVIDUAL   NERVES   AND   PLEXUSES.      265 

Symptoms. — The  symptoms  of  hepatic  colic  are  more  or  less  severe 
pain  which  comes  on  suddenly  and  lasts  with  irregular  intermissions  and 
exacerbations  from  a  few  hours  to  a  few  days.  The  pain  is  often  very 
severe,  and  of  an  aching,  cutting,  or  tearing  character,  and  is  usually 
attended  with  a  feeling  of  constriction  or  cramp.  It  is  o-enerallv 
referred  to  the  pit  of  the  stomach  or  to  the  umbilicus,  whence  it  radiates 
to  the  back  and  between  the  shoulders,  but  never  downwards.  The 
patient  suffers  during  a  severe  attack  from  faintness,  nausea,  and  vomit- 
ing ;  the  action  of  the  heart  is  Aveakened,  the  surface  of  the  body  is 
cold,  and  in  severe  cases  there  are  symptoms  of  collapse. 

(\  Neu7'algia  Hypog<(strica. 

Hyposastric  neuralgia  mav  be  divided  into  the  followino-  varieties 
according  to  the  branches  of  the  plexus  affected, 

(1)  Neuralgia  Ani. 

Etiology. — Neuralgia  of  the  rectum  generally  results  from  fissures  of 
the  anus,  but  it  may  occur  in  the  absence  of  any  recognizable  local 
cause ;  and  it  is  a  common  symptom  of  locomotor  ataxia. 

Symptoms. — The  symptoms  consist  of  severe  paroxysms  of  cutting 
pains  coming  on  suddenly  and  si)ontaneously  after  exposure  to  cold. 
The  pains  are  situated  an  inch  within  the  anus,  and  they  are  much  in- 
creased by  defecation.  The  pain  is  associated  with  hypersesthesia  or 
an;esthesia  of  the  skin  of  the  perineal  region,  spasm  of  the  sphincter 
ani  and  bladder,  and  difficulty  of  micturition. 

(2)  Neuralgia  Uteri  (Hysteralgia). 

Etiology. — The  causes  of  uterine  neuralgia  are  prolapse  of  the  uterus, 
uterine  tumors  of  all  kinds,  ulceration  of  the  cervix,  profuse  and  in- 
tractable leucorrhoea,  ascarides  in  the  rectum,  scybala  impacted  in  the 
rectum,  and  calculus  in  the  ureter  or  kidney.  Sometimes  the  source  of 
irritation  may  be  in  a  remote  part  of  the  body,  and  in  some  cases 
paroxysms  of  uterine  neuralgia  may  occur  in  the  absence  of  any  dis- 
coverable disease  of  the  pelvic  organs. 

Symptom,s. — The  patient  complains  of  paroxysmal  attacks  of  intense 
pain  situated  deeply  in  the  pelvis  which  is  aggravated  by  movement, 
by  the  maintenance  of  the  erect  posture,  and  by  pressure  on  the  cervix. 
The  pain  often  radiates  to  the  inguinal  and  lumbar  regions  of  one  si<le, 
and  it  is  often,  although  not  always,  worse  at  the  menstrual  period. 


2(36  DISORPERS    OF    MIXED    NERVES. 

Vaginismus  is  a  condition  of  excessive  sensibility  of  the  vaginal 
orifice  which  renders  coitus  impossible.  It  is  often  associated  with 
spasm  of  the  constrictor  vagina  and  of  the  levator  ani,  and  attempts  at 
coition  may  induce  general  hysterical  convulsions. 

(3)  Ovarian  Neuralgia  axd  Hyper.esthesia  (Ovarialgia). 

Miolof/i/.—OvaYian  neuralgia  may  be  caused  by  any  of  the  sources 
of  irritation  already  enumerated  as  the  causes  of  uterine  neuralgia. 
The  left  ovary  is  the  one  usually  aflFected.  It  is  frequently  associated 
-with  o-rave  hysterical  symptoms,  and  it  is  difficult  to  determine  whether 
the  ovarian  pain  is  to  be  regarded  as  the  cause  or  an  effect  of  the 
hysteria. 

St/mptoms. — The  symptoms  of  ovarian  neuralgia  consist  of  pain, 
which  is  sometimes  so  acute  that  the  patient  cannot  tolerate  the  slightest 
touch,  and  which  is  localized  partly  in  the  hypogastrium  and  partly  in 
the  iliac  fossa.  In  many  cases  there  is  more  or  less  complete  anesthesia 
of  the  abdominal  walls  and  pain  is  only  elicited  on  deep  pressure  over 
the  affected  ovary,  which  c-in  generally  be  felt  by  the  hand  in  the  other 
variety  of  ovarian  neuralgia.  Pressure  exaggerates  this  iliac  pain,  and 
causes  it  to  radiate  towards  the  epigastrium  and  throat.  The  radia- 
tion of  the  pain  towards  the  epigastrium  is  often  accompanied  by  nausea 
and  vomiting,  and,  if  the  pressure  be  continued,  palpitations  of  the 
heart,  increased  frequency  of  the  pulse,  and  a  sensation  of  "  globus 
hystericus"  supervene.  If  the  pressure  be  continued,  the  patient, 
according  to  Charcot,  suffers  on  the  affected  side,  in  addition  to  the 
symptoms  just  described,  from  l(»ud  sibilant  sounds  in  the  ear,  obscurity 
of  the  sight  of  the  eye,  and  a  sensation  as  of  blows  from  a  hammer  on 
the  temporal  region. 

(4)  Neuralgia  Testis. 

Etiology. — Neuralgia  of  the  testis  may  be  caused  by  morbid  growths 
in  the  organ,  and  calculus  in  the  ureter,  while  it  is  not  uncommon  in 
neurotic  subjects  as  the  result  of  self-abuse. 

Symptoms. — The  symptoms  of  neuralgia  of  the  testis  consist  of 
spontaneously  arising  paroxysms  of  severe  pain  which  is  situated  partly 
in  one  testicle  and  partly  in  the  epididymis  and  cord.  The  organ  is 
tender  to  pressure  and  contact,  and  the  patient  complains  of  a  dull 
aching  pain  in  the  intervals  between  the  paroxysms.  During  the 
paroxysm  the  testicle  is  strongly  retracted  from  spasm  of  the  cremaster 
muscle,  and  the  patient  suffers  from  fainting  and  vomiting.  The  affec- 
tion is  usually  very  obstinate,  and  it  is  often   accompanied  by  great 


DISORDERS    OF    THE    NERVES    OF    SPECIAL    SENSE.      267 

mental  depression   which   may   end    in    confirmed  hypochondriasis  or 
melancholia. 

(5)  Cystalgia. 

Etiology. — Neuralgia  of  the  bladder  usually  results  from  the  presence 
of  calculus,  or  malignant  disease,  but  it  occasionally  results  in  -women 
from  long-continued  menorrhagia  combined  Avith  anaemia. 

Symptoms. — Neuralgia  of  the  bladder  consists  of  severe  paroxysms 
of  pain,  which  is  situated  at  the  neck  of  the  bladder,  and  is  accompanied 
by  a  frequent  desire  to  micturate. 

(d)  Neuralgia  Urethralis. 

Etiology. — Neuralgia  of  the  urethra  may  occur  in  the  absence  of  any 
local  source  of  irritation,  and  is  then  generally  a  symptom  of  locomotor 
ataxia. 

Symptoms. — Neuralgia  of  the  urethra  consists  of  paroxysms  of  severe 
pain  in  the  course  of  the  urethra.  The  pain  is  accompanied  by  an 
urgent  desire  to  pass  water,  probably  caused  by  spasm  of  the  detrusor 
muscle,  but  the  patient  frequently  experiences  difficulty  in  voiding  the 
urine,  probably  because  the  sphincter  is  also  spasmodically  contracted. 


IV.    DIKOEDERS  OF  THE  NERVES  OF   SPECIAL  SENSE. 

1.  Diseases  of  the  Olfactory  Nerve. 

The  sense  of  smell  is  excited  by  the  contact  of  odoriferous  particles 
with  that  part  of  the  mucous  membrane  of  the  nose  to  which  the  olfoc- 
tory  nerves  are  distributed.  The  smell  induced  by  simple  diffusion  of 
odoriferous  particles  is  very  imperfect,  but  the  sensation  is  much  in- 
tensified by  the  forcible  impact  of  those  particles  against  the  mucous 
membrane  which  is  obtained  by  the  process  of  sniffiyig. 

Tests. — In  testing  the  sense  of  smell  care  should  be  taken  not  to 
irritate  the  fifth  nerve,  and  conse(iuently  substances  having  a  pungent 
odor  should  be  avoided.  The  best  substances  are  volatile  oils,  the  fetid 
gum  resins,  and  other  substances  having  a  penetrating  odor  like  cam- 
phor and  musk.  Our  perception  of  flavors  being  due  to  the  sense  of 
smell  and  not  to  that  of  taste,  it  is  necessary  to  get  the  patient  to  par- 
take of  substances  possessing  a  delicate  aroma  or  bouquet,  such  as  roast 
beef,  cheese,  or  wine.  Electricity  is  not  of  much  use  in  testing  the 
sense  of  smell. 


208  DISORDERS    OF    CRANIAL    NERVES. 

a.  Hyperosmia  or  Olfactory  Hyperesthesia. 

The  acuteness  of  the  sense  of  smell  may,  like  that  of  the  other 
senses,  be  increased  by  education,  and  hysterical  patients  are  often  able 
to  discriminate  smells  which  are  quite  inappreciable  to  others. 

h.  Hyperalgesia  of  the  Sense  of  Smell. 

The  sense  of  smell  is  fre(iuently  perverted  in  insanity,  and  other 
grave  diseases  of  the  nervous  system.  Hysterical  subjects  may  mani- 
fest a  decided  aversion  to  perfumes  which  are  agreeable  to  most  people, 
or  a  predilection  for  odors,  like  that  of  asafoetida,  which  are  repugnant 
to  others.  An  unaccountable  aversion  to  a  particular  perfume  is  some- 
times one  of  the  earliest  symptoms  of  locomotor  ataxia. 

Illusions  or  hallucinations  of  smell,  which  are  generally  of  a  repug- 
nant kind,  are  often  complained  of  by  the  insane.  The  most  usual 
odors  complained  of  are  those  of  sulphur  and  putrid  substances,  and 
these  patients  are  often  led  to  believe  that  they  arc  surrounded  Ijy  dead 
and  decaying  bodies.  A  bad  smell  sometimes  constitutes  the  aura  of 
epileptic  and  epile|)tiform  seizures,  and  it  may  likewise  be  a  symptom 
of  an  intracranial  tumor. 

c.  Anosmia  or  Olfactory  Ancesthesia. 

Anosmia  consists  of  a  diminution  or  complete  loss  of  the  sense  of 
smell,  and  when  both  sides  are  affected  the  sense  of  taste  is  likewise 
impaired.  The  sense  of  smell  is  diminished  in  disease  of  the  fifth 
nerve  owing  to  nutritive  changes  occurring  in  the  mucous  membrane 
of  the  nose,  and  it  is  also  diminished  in  fiicial  paralysis  l)ecause  the  act 
of  sniffing  becomes  impossible,  owing  to  the  paralysis  of  the  dilators  of 
the  alas  nasi.  It  is  likewise  impaired  by  local  disease,  such  as  constric- 
tion of  the  nostrils,  nasal  polypi,  acute  and  chronic  inflammation  of  the 
mucous  membrane,  strumous  and  syphilitic  oz8ena,  and  occlusion  of 
the  nasal  and  pharyngeal  cavities.  The  sense  of  smell  is  frequently 
blunted  in  old  age,  and  loss  of  smell  is  occasionally  observed  as  an  early 
and  persistent  symptom  of  locomotor  ataxia.  Loss  of  smell  is  some- 
times caused  by  injuries  of  the  head,  the  affection  being  thus  described  as 
traumatic  anosmia.  The  most  frequent  injury  to  cause  anosmia,  in  the 
absence  of  fracture  of  the  cranium,  is  a  blow  or  fall  on  the  occiput,  and 
a  blow  on  the  forehead  is  sometimes  followed  by  loss  of  smell.  Anos- 
mia of  the  left  nasal  cavity  is  sometimes  associated  with  right  hemi- 
plegia and  aphasia,  the  result  of  embolism  of  the  middle  cerebral  artery. 


' 


DISORDEKS    OF    THE    NEEVES    OF    SPECIAL    SENSE.      269 

In  Other  cases  left-sided  anosmia  is  associated  Avith  aphasia  in  the 
absence  of  any  paralysis,  and  in  some  of  these  cases  at  least  the  dis- 
order of  speech  Avas  a  sensory  aphasia.  In  cerebral  hemiana-sthesia, 
Avhether  of  hysterical  origin  or  caused  by  organic  disease,  smell  is  lost 
on  the  same  side  as  the  other  sensory  disorders.  Loss  of  smell  is  also 
caused  by  tumors  in  the  anterior  fossa  of  the  skull,  or  in  the  anterior 
cerebral  lobes,  and  by  basal  meningitis,  exostoses,  or  caries  of  the  bones. 
It  is  at  other  times  a  congenital  affection,  and  then  usually  results  from 
absence  of  the  olfactory  bulbs. 

3Iorhid  Anatomy  and  Physiology. — Diminution  or  loss  of  smell  may 
be  caused  by  disease  of  the  local  olfactory  organ,  the  peripheral  end- 
oi'gans,  the  olfactory'  nerves,  the  conducting  apparatus  through  the 
olfactory  bulbs  and  hemispheres  of  the  brain,  or  of  the  cortical  centres 
themselves.  With  regard  to  local  disease  it  Avill  suffice  to  say,  that  it 
is  very  probable  the  ramifications  of  the  olfactory  nerves  themselves 
become  secondarily  affected  in  chronic  inflammation  and  other  diseases 
of  the  mucous  membrane.  Loss  of  smell  may,  however,  be  caused  by 
disease  of  the  peripheral  end-organs  of  tlie  olfactory  nerve  in  the 
absence  of  disease  of  the  mucous  membrane.  Smell  is  sometimes 
permanently  lost  in  consequence  of  the  impression  of  a  very  powerfid 
stench,  and  Prevost  found  degeneration  of  the  olfectory  nerves  and 
atrophy  of  the  bulbs  in  old  people  in  Avhom  the  sense  of  smell  Avas 
diminished.  The  anosmia  Avhich  accompanies  locomotor  ataxia  is  caused, 
most  probably,  by  a  neuritis  of  the  olfactory  nerves,  AN'hile  that  Avhich 
accompanies  cerebral  tumors  is  most  frequently  caused  by  compression 
of  the  olfactory  nerves  and  bulbs.  Traumatic  anosmia  is  generally 
caused  by  bloAvs  on  the  occiput ;  the  elastic  bones  of  the  cranium  yield 
to  some  extent  to  the  bloAv;  the  Avhole  of  the  encephalon  above  the  ten- 
torium is  thus  pushed  forAvards ;  the  anterior  margins  of  the  temporo- 
sphenoidal  lobes  impinge  against  the  great  Avings  of  the  sphenoid  bones  : 
and  the  olfactory  bulbs  are  apt  to  suffer  damage  at  these  points  of  junc- 
tion ANitli  the  brain  near  the  anterior  perforated  space,  or  some  of  the 
olfactory  nerves  may  be  ruptured  in  their  passage  through  the  cribriform 
plate  of  the  ethmoid  bone. 

2.  Diseases  of  the  Acoustic  NERyES. 

a.  Auditory  Hypercesthesia  or  Hyperacusia. — In  this  condition  the 
sensibility  of  the  auditory  sensory  mechanism  is  increased,  so  that 
sounds  too  faint  to  be  detected  in  the  normal  state  are  heard  distinctly, 
A\hile  the  poA\'er  of  discriminating  differences  in  sounds  is  unusually 
acute.      Hyperacusia  is  often  observed  in  hysterical  patients,  in  con- 


270  DISORDEES    OF    CRAXIAL    NERVES. 

(litions  of  ecstacy,  and  sometimes  even  in  somnambulism.  Auditory 
hypergesthesia,  however,  generally  declares  itself,  not  by  an  increased 
power  of  discriminating  tones,  but  an  increase  of  the  pleasant  or  painful 
feelino-s  which  accompany  sound,  and  this  condition  may  be  called  audi- 
tory hyperalgesia.  In  disease  the  painful  feelings  which  accompany 
sound  predominate,  and  in  cases  of  acute  disease,  general  debility,  hys- 
teria, and  various  mental  affections,  the  slightest  sound  becomes  exceed- 
ingly distressing  to  the  patient.  Auditory  hyperaesthesia  is  often  accom- 
panied by  subjective  sensations,  illusions,  and  hallucinations.  Tinnitus 
is  the  most  common  form  of  subjective  sensation,  and  it  may  assume  the 
form  of  whistling,  humming,  and  various  other  noises.  This  symptom 
is  generally  caused  by  disease  of  the  external  or  middle  ear,  changes  in 
the  circulation  of  the  brain,  large  doses  of  quinine  or  salicin,  and 
forms  a  prominent  feature  of  Meniere's  disease.  Auditory  illusions 
are  frequently  observed  in  mental  disease,  more  especially  in  melan- 
cholia and  dementia ;  in  the  former  they  assume  the  form  of  abusive 
or  threatening  words  or  commands  to  do  acts  of  violence,  and  in  the 
latter  they  take  the  form  of  heavenly  messages  or  revelations.  Audi- 
tory illusions  are  sometimes  unilateral,  and  in  some  cases  there  are 
alternating  illusions  of  different  senses,  such  as  right-sided  optic  and 
left-sided  auditory  illusions.  Auditory  hallucinations  sometimes  con- 
stitute the  aura  of  an  epileptic  attack.  The  galvanic  current  affords 
valuable  aid  in  the  diagnosis  of  the  various  conditions  of  the  auditory 
nerve,  but  for  information  on  this  subject  the  reader  is  referred  to 
special  treatises. 

h.  Auditory  anaesthesia  consists  of  abnormal  diminution  or  abolition 
of  the  sense  of  hearing.  The  cause  of  deafness  may  be  either  lesion 
of  the  local  apparatus  of  hearing  and  of  the  peripheral  nerve-endings, 
of  the  conducting  apparatus,  or  of  the  central  terminal  organ.  Func- 
tional deafness  is  observed  in  hysteria,  and  after  toxic  doses  of  quinine, 
lead,  and  other  agents. 

3.  Diseases  of  the  Gustatory  Nerves. 

The  gustatory  nerves  are  derived  from  the  glosso-pharyngeal  nerve 
(Fig.  84)  which  supplies  fibres  to  the  posterior  third  of  the  tongue,  the 
palate,  and  the  walls  of  the  pharynx ;  and  from  the  lingual  branches 
of  the  fifth  nerve,  which  are  distributed  to  the  tip  and  anterior  two- 
thirds  of  the  tongue.  It  has  been  proved  by  experiment  and  by  an 
analysis  of  clinical  observations  that  most,  if  not  all,  of  the  gustatory 
fibres  of  the  lingual  nerve  are  derived  from  the  chorda  tympani ;  this 
nerve  joins  the  fiicial  in  the  Fallopian  canal,  but  on  reaching  the  genicu- 


DISORDERS    OF    THE    NERVES    OF    SPECIAL    SENSE.      271 


late  ganglion  the  gustatory  fibres  leave  the  facial  and  return  by  means 
of  the  petrosal  nerves  to  the  trigeminus,  with  which  they  enter  the 
cavity  of  the  skull  and  brain.  Gowers  believes  that  the  gustatory  fibres 
of  the  glosso-pharyngeal  are  also  derived  from  the  fifth  nerve. 


Fig.  84. 


GP, 
1, 


To 


DiAGRA^M  OF  Glosso-pharyngeal  Xerve,  its  Connections  and  Branches. 
(From  Hermann's  "PLj'siologj-.") 
Glosso-pharyngeal  nerve.     JG,  Its  jugular  ganglion.     PG,  Its  petrous  ganglion. 
Tympanic  branch,  or  nerve  of  Jacobson,  the  branches  of  which  are  as  follows  : 
2,  Filaments  to  plexus  on  carotid  artery  ;    3,    To  Eustachian  tube ;    4,  To  fenestra  rotunda  ; 
fenestra  ovalis. 

6,  Twig  of  union  with  small  superficial  petrosal  n. 

7,  Twig  of  union  with  great  su^yerficial  petrosal  n. 
S,  Pharyngeal  branches  of  glosso-pharyngeal  n. 

9,  Muscular  branches  to  stylo-pharyngeus  and  constrictors  (?). 

10,  Tonsillitie  branches. 

11,  Terminal  lingual  branches. 

P,  Pneumogastric  nerve,  from  the  ganglion  of  the  root  of  which,  branches  pass  to  the  petrous  ganglion. 
S,  Superior  cervical  ganglion  with  an  ascending  branch  to  the  petrous  ganglion. 
MG,  Meckel's  ganglion.     OG,  Otic  ganglion.     F,  Facial  nerve.     CA,  Carotid  artery. 

Tests  of  the  Sense  of  Taste. — The  patient  should  be  directed  to  put 
his  tongue  out,  with  the  mouth  widely  open  and  the  eyes  closed,  and  then 


272  DISORDEES    OF    CKAKIAL    NERVES. 

the  sapid  substance  is  applied,  with  a  glass  rod  or  small  lirush,  to  the 
part  to  be  tested.  The  tongue  ought  not  to  be  withdrawn  into  the 
mouth  until  time  is  given  for  the  taste  to  be  perceived. 

Bitter  tastes  are  most  distinctly  perceived  at  the  root  of  the  tongue, 
and  they  may  be  tested  by  a  solution  of  quinine  or  infusion  of  quassia. 
Sweet  tastes  are  best  perceived  at  the  tip  of  the  tongue  and  are  tested 
by  syrup  or  honey.  Acids  and  salines  are  most  readily  perceived  at 
the  sides  of  the  tongue  and  are  tested  by  vinegar  and  solution  of  common 
salt.  Galvanization  of  the  tongue  by  means  of  special  electrodes  is 
also  a  valuable  method  for  testing  the  sense  of  taste. 

a.  Ilypera^sthesia  of  the  Gustdtory  Nerves. 

Hypen^sthesia  of  the  sense  of  taste  may  manifest  itself  as  an  increase 
in  the  delicacy  of  taste.  Hysterical  patients,  for  example,  often  detect 
certain  ingredients  in  food  or  medicines  which  are  quite  inappreciable 
to  healthy  persons.  It  may  again  express  itself  as  an  increase  in  the 
enjoyment  or  loathing  of  food,  certain  substances  causing  a  more  agree- 
able or  disgusting  taste  than  they  do  in  the  case  of  the  healthy  palate. 
Amongst  the  parcesthesia  must  be  mentioned  the  subjective  sensations 
of  taste  perceived  on  the  anterior  half  of  the  tongue  in  some  cases  of 
facial  paralysis,  and  when  certain  drugs  have  been  taken.  The  subjec- 
tive gustatory  sensations  of  insane  patients  are,  doubtless,  of  centric 
origin,  and  consist  partly  of  hallucinations,  and  i)artly  of  illusions  of 
taste. 

b.  Ancesthesia  of  the  Gustatory  Nerves. 

(xustatory  anaesthesia  may  be  complete  or  incomplete  in  its  degree, 
circumscribed  or  diffused  in  extent,  and  partial  or  total  as  regards  the 
forms  of  sapid  qualities  interfered  with. 

Gustatory  anaesthesia  maybe  caused  by  catarrh  or  other  local  disease, 
or  by  lesion  of  the  glosso-pharyngeal,  lingual,  chorda  tympani,  facial, 
or  trigeminal  nerves.  When  the  glosso-pharyngeal  nerve  is  affected  taste 
is  weakened  or  lost  on  the  root  of  the  tongue,  palate,  and  pharynx  on 
the  corresponding  side,  but  no  uncomplicated  case  of  this  kind  is  yet 
recorded.  Little  is  known  with  regard  to  disease  of  the  cortical  centres 
of  taste.  If  the  lesion  is  situated  on  the  lingual  or  chorda  tympani 
nerves,  or  in  certain  sections  of  the  facial  or  trigeminal  nerves,  the 
gustatory  aneesthesia  affects  the  anterior  or  lateral  half  of  the  tongue 
along  with  its  border  and  apex.  When  loss  of  taste  in  the  areas  of  dis- 
tribution of  the  lingual  and  glosso-pharyngeal  nerves  of  one  side  is 
associated  with  hemianeesthesia  of  the  same  side  of  the  body,  it  may  be 


DISORDERS    OF    THE    NKRVES    OF    SPECIAL    SEXSE.       "JTS 

inferred   that   the   lesion  is  central,  such   a  combination   of  symptoms 
being-  generally  met  with  in  hysteria. 


4.  Diseases  of  the  Optic  Nerves. 

<i.  Functional  Affections  of  the  Sense  of  Si(//tt. 

(1)  Optic  Hypkr.esthksia  ano  Hyperalgesia. 

Optic  hypersesthesia  consists  of  those  conditions  in  which  external 
objects  are  distinctly  seen  in  an  obscure  light,  or  in  which  the  acuteness 
of  vision  is  greater  than  in  ordinary  sight.  But  disease  usually  drives 
rise  to  painful  feelings  or  to  abnormal  psychical  visual  sensations,  such 
as  sparks  of  light  and  luminous  disks,  and  these  may  be  comprised 
under  the  name  of  optic  hyperalgesia.  Illusions  and  hallucinations  of 
sight  occur  in  insanity,  epilepsy,  and  vai-ious  other  cerebral  affections. 

(2)  Optic  An.esthe.sia. 

Optic  anaesthesia  is  characterized  by  diminution  of  vision  or  Kinbly- 
opia.,  or  ])y  abolition  of  vision  or  atnaurosix. 

Etiologij — The  forms  of  amblyo{)ia  and  amaurosis  which  occur  in  the 
absence  of  any  apparent  lesion  of  the  fundus  of  the  eye  on  ophthal- 
moscopic examination  are  those  which  interest  us  at  present.  Amblyopia 
or  even  amaunjsis  is  sometimes  caused  Ijy  exposure  to  cold,  venereal 
excesses,  exhaustion,  hsematemesis,  profuse  menorrhagia,  or  other  severe 
loss  of  blood,  irritation  of  the  sensory  branches  of  the  trigeminus,  and 
irritation  of  the  abdominal  organs  by  the  presence  of  worms,  constipa- 
tion, tumors,  pregnancy,  or  uterine  disease.  An  epileptic  attack  may 
be  succeeded  by  a  temjiorary  enfeeblement  of  sight,  which  usually  dis- 
appears rapidly,  but  may  become  more  or  less  pennanent  when  the 
attacks  are  frequently  repeated.  Unilateral  blindness,  lasting  only  for 
a  few  minutes,  may  occur  in  paroxysms  in  the  midst  of  perfect  health, 
and  it  may  possibly  be  regarded  as  a  vaso-motor  epilepsy.  Amblyopia 
may  result  from  toxic  agents  such  as  lead,  alcohol,  tobacco,  opium, 
belladonna,  quinine,  and  santonin,  or  it  may  be  a  se([uel  of  acute 
diseases,  like  typhus  fever,  scarlet  fever,  and  pneumonia. 

Symptoms. — The  symptoms  of  functional  amblyopia  and  amaurosis 
are  the  same  as  those  which  are  observed  in  organic  diseases  of  the  optic 
nerves,  except  that  in  the  former  no  changes  are  found  in  the  fundus 
on  ophthalmoscopic  examination. 

Vision  presents  four  distinct  alterations  in  amblyopia :  {a)  Diminution 
in  the  acuteness  of  vision;   (6)  Alterations  in  the  field  of  vision;  {>■) 

18 


274  PISOBDERS    OF    CRAXIAL    XERVES. 

Disorders  in  the  perception  of  light ;  and  {d)  Disorders  in  the  percep- 
tion of  colors. 

(a)  Diminution  in  the  Acutenes^  of  Vision.— "iXie  patient  sees  objects 
through  a  mist ;  he  has  difficulty  in  distinguishing  minute  objects,  or 
at  times  may  observe  a  dark  spot  in  the  centre  of  vision. 

Tests  of  the  Acuteness  of  Visio?!.— The  acuteness  of  vision  is  usually 
tested  by  asking  the  patient  to  read  print  of  a  certain  size  of  type,  and 
at  definite  distances.  In  Snellen's  scale  the  size  of  type  is  numbered 
according  to  the  distance  in  feet  at  which  the  print  can  be  read  by  the 
normal  eye  in  a  good  light.  The  acuteness  of  vision  is  expressed  by  a 
fraction  of  which  the  denominator  is  the  number  of  the  test  type,  and 
the  numerator  the  distance  in  feet  at  which  it  can  be  read.  The  sight 
of  each  eye  must  always  be  tested  separately. 

(b)  Alterations  in  the  Field  of  Vision. — The  field  of  vision  may  be 
altered  in  several  ways,  but  the  form  usually  observed  in  functional 
amblyoi)ia  begins  at  the  margin  of  the  field  and  progresses  concentri- 
cally until  only  a  small  central  area  is  left.  The  first  loss  of  vision 
may  appear  in  the  centre  of  the  field,  constituting  a  central  scotoma, 
while  at  times  the  whole  field  of  vision  is  covered  with  scotomata.  The 
blindness  may  sometimes  be  surrounded  by  spectral  appearances  and 
then  it  is  named  a  scintillatinc)  scotoma.  In  their  simplest  form  they 
consist  of  a  blind  area  which  is  surrounded  more  or  less  completely  l)y 
a  luminous  border,  the  latter  Avidening  as  the  former  expands.  This 
luminous  arc  is  subject  to  a  rapid  oscillatory  movement  which  has  been 
variously  described  by  different  observers.  In  the  more  pronounced 
forms  the  luminous  border  assumes  a  zigzag  outline  which  has  been 
compared  to  the  outlines  of  a  fortification.  It  is  also  fringed  l)y  gorgeous 
colors  which  are  in  continual  trembling  movement,  or  appear  to  ''corus- 
cate," or  to  emit  a  "shower  of  sparks."  The  phenomenon  lasts  from 
a  quarter  to  half  an  hour  and  then  passes  off". 

Tests  of  the  Field  of  Vision. — The  most  ready  test  of  the  field  of  Aision 
is  to  direct  the  patient  to  fix  one  eye,  the  other  being  closed,  on  the 
corresponding  eye  of  the  operator,  and  the  latter  then  moves  his  hand 
to  the  right,  left,  above,  and  below,  and  at  a  certain  distance  from  the 
fixed  point  as  a  centre.  If  the  field  of  vision  be  limited  in  any  particu- 
lar direction,  the  observer  will  have  to  approach  his  hand  nearer  and 
nearer  to  the  point  on  which  the  patient's  eye  is  fixed  before  it  is  seen, 
and  thus  any  serious  departure  from  the  normal  limit  can  be  readily 
detected.  If  greater  accuracy  be  required,  the  field  must  be  measured 
by  means  of  the  "  mapping  system  "  or  by  the  perimeter,  for  a  descrip- 
tion of  which  the  reader  is  referred  to  ophthalmological  works. 


DISORDEKS    OF    THE    XERVES    OF    SPECIAL    SKX3E.       27." 


::LiO 


(c)  Disorders  of  the  Perception  of  Light.  —  There  are  several 
varieties  of  partial  anaesthesia  in  which  the  ophthalmoscopic  appearance 
may  be  negative.  Sometimes  the  patient  cannot  see  at  night,  a  condi- 
tion which  is  called  henwralopia ;  at  other  times  sight  is  deficient  in 
daylight,  and  this  condition  is  called  nyetalopia. 

(d)  Disorders  of  the  Pereeption  of  Colors  {Dyschromatopsia,  Achro- 
matopsia).— The  perception  of  colors  may  be  defective  when  the  acutencss 
of  vision  is  very  little  impaired,  and,  conversely,  color  vision  may  be 
little  aflected  when  there  is  considerable  limitation  of  the  field  of  vision. 
The  area  of  the  field  of  vision  varies  for  each  color,  green  havino-  the 
smallest  and  yellow  and  blue  the  largest  visible  areas  (Fig.  85). 

Fig.  85. 


DiAiiRAU  Showing  the  Fiklds  of  Color  Vision  in  a  Normal  Emmetropic  Eye  on  a  Dim.  Day. 

(After  GowERS.) 

Tlie  fields  are  each  ratliei-  smaller  than  on  a  bright  day.     The  asterisk  indicates  the  fixing-  point,  the 

black  dot  the  position  of  the  blind  spot.     (U.sually  the  blue  field  is  larger  than  the  yellow.) 

Tests  of  Color  Vision. — A  scale  of  colors  is  submitted  to  the  patient 
and  it  must  be  ascertained  whether  he  can  identify  and  name  each ;  or 
the  patient  is  asked  to  match  a  given  color  from  a  number  of  others 
presented  to  him. 

In  amblyopia  the  order  in  which  the  percej)tion  of  colors  is  lost  is 
usually  that  in  which  the  fields  are  arranged  on  the  retina,  the  first 
defect  beino;  for  o-reen,  then  red,  while  yellow  and  blue  are  the  last  to 
be  lost.  The  condition  in  which  central  vision  for  the  perception  of  one 
or  more  colors  is  much  restricted  is  named  dyschromatopsia,  while  total 
color  blindness  is  named  achromatopsia. 

Color  blindness  is  sometimes  a  congenital  defect,  and  of  tins  form 
there  are  three  varieties;  namely,  (1)  Red  blindness,  (2)  (irecii  blind- 


276  DISOKDEKS    OF    CRANIAL    NERVES. 

uess,  and  (^J)  Violet  blindness.  Dalton  suffered  from  red-blindness  ;  he 
imagined  that  diluted  ink  gave  a  color  much  resembling  a  florid  com- 
plexion ;  blood  appeared  to  him  not  unlike  in  color  to  that  called  bottk-- 
areen  •  and  he  could  not  distinguish  between  the  color  of  a  ripe  cherry 
and  that  of  a  leaf. 

b.    Orjiiinic  Bisi'ases  of  the  OjJtic  JVcrvc^. 
Optic  Neuritiif:  and  Atrophy. 

Etiology. — Ojitic  neuritis  may  l)e  caused  by  tumors  of  the  brain, 
hydrocephalus,  basal  meningitis,  meningeal  hemorrhages,  and  throm- 
bosis of  the  cavernous  sinus,  but  it  only  rarely  results  from  abscess  of 
the  brain,  and  softening  from  occlusion  of  vessels,  and  in  the  few  cases 
in  Avliich  it  was  associated  with  hemorrhage  it  may  be  suspected  that  a 
tilioma  was  jjresent.  Optic  neuritis  is  occasionally  observed  in  cases 
in  which  the  symptoms  point  to  intracranial  disease,  but  in  which  the 
])ost-mortem  examination  reveals  no  lesion.  It  may  also  be  caused  by 
extracranial  causes,  such  as  orbital  tumors,  and  inflammation  of  the 
bones,  periosteum,  or  cellular  tissue  of  the  orbit,  and  hyperostosis  nar- 
roAving  the  optic  foramina.  Optic  neuritis  sometimes  follows  injuries 
of  the  cervical  spine,  while  it  has  occasionally  been  observed  in  caries 
of  the  cervical  vertebrit;,  witli  transverse  myelitis  of  the  cervical  and 
dorsal  regions  of  the  cord. 

Double  optic  neuritis  is  sometiuics  caused  by  acute  diseases,  suc-h  as 
the  specific  fevei's  and  pneumonia.  I'Xposure  to  C(dd  or  to  a  very  bright 
light,  suppression  of  the  menses,  or  chronic  blood-poisoning  from  lead, 
syphilis,  diabetes  niellitus,  or  chronic  liright's  disease. 

Varieties. — The  diseases  of  the  optic  nerves  may  divided  as  follows  : 

(1)  Congestive  and  inflammatory  affections  : 
(a)  Simple  congestion  of  the  disk. 

{b)  Congestion  with  swelling  of  the  disk  (optic  neuritis). 
((')  Albuminuric  retinitis  and  neuritis. 

(2)  Atrophic  affections: 

(a)  Simple  or  primary  atroj)hy. 
{b)  Secondary  atrophy. 

(1)  Inflammatory  Affections  of  thk  Optic  Nerve. 

{'()  Simple  congestion  is  characterized  by  an  increased  redness  of 
the  disk,  Avhich  is  the  more  readily  recognized  when  it  is  greater  in 
one  eye  than  in  the  other.  The  redness  invades  the  })hysiological  cup 
and  may  entirely  obscure  it;  the  sclerotic  ring  and  the  edge  of  the 
choroid  are  rendered  indistinct,  and  the  disk  loses  its  sharpness  of 
outline. 


DISORDERS    OF    THE    XEKVES    OF    SPECIAL    S  K  X  S  E .       277 

(/>)  Optic  neuritis  is  characterized  b}'  (edema  as  well  as  congestion  of 
the  disk,  which  becomes  enlarged,  swollen,  red,  and  cloudy,  the  physio- 
logical cup  is  obscured,  the  sclerotic  ring  and  the  edge  of  the  choroid 
are  concealed,  and  the  edges  of  the  disk  are  l)adly  defined  and  hazv. 
As  the  disease  advances  the  disk  becomes  more  swollen,  it  assumes  a 
reddish-grav  color,  and  its  periphery  becomes  distinctly  striated,  partly 
owing  to  the  swelling  and  opacity  of  the  nerve  fibres  and  partly  to  an 
enormous  development  of  minute  vessels.  The  veins  are  enororored 
tortuous,  and  often  varicose,  while  the  arteries  are  reduced  in  size,  and 
a])pear  paler  than  the  veins,  ^Vhen  exudation  takes  place  the  vessels 
become  veiled  and  lost  to  sight  at  the  boi'der  of  the  disk,  but  reappear 
partially  as  they  proceed  inwards,  and  disappear  again  l)efore  reaching 
the  lamina  cribrosa. 

The  inflammaticm  may  now  subside,  the  swelling  gradually  dimin- 
ishes, the  edge  of  the  choroid  becomes  apparent,  and  the  only  indica- 
tion of  the  previous  inflammation  which  remains  may  be  a  narrow  zone 
of  atmphy  adjacent  to  the  disk  and  along  the  edge  of  the  choroid. 

(j)  I:J)i;/07yed  or  Choked  Disk. — If  the  inflammation  continues  the 
<lisk  becomes  still  more  swollen,  and  its  margins  becoming  steeper,  the 
vessels  which  pass  over  the  side  become  concealed  by  the  edge  of  the 
swelling,  and  reappear  in  a  different  position  in  the  fundus.  The 
arteries  are  reduced  to  small  threads  and  are  often  invisible,  but  the 
veins  ai-e  visible  towards  the  edge  of  the  tumor  and  often  appear  dis- 
tended and  tortuous  for  a  long  distance  fi'om  the  disk.  Hemon-hages 
are  now  frequent  and  extensive,  and  generally  ajjpear  at  the  edge 
rather  than  on  the  surface  of  the  swelling.  Sight  becomes,  as  a  ride, 
rapidly  impaired  during  this  stage  of  strangulation.  This  form  of 
neuritis  has  been  called  the  choked  <>r  engorged  disk. 

(jj)  Subsidence  of  Optic  Neuritis. — After  the  strangulation  has 
existed  for  some  time  the  veins  become  less  distended,  the  swelling  loses 
its  intense  red  color  and  becomes  pale  and  less  prominent,  hemorrhages 
cease,  the  extravasated  blood  is  absorbed,  leaving  pigmented  or  white 
spots  on  the  retina,  the  edges  of  the  choroid  and  the  sclerotic  ring 
become  dimly  apparent  after  a  time,  and  then  the  (hsk  assumes  a 
whitish  or  grayish  color,  its  edges  being  generally  irregulai-  and  sur- 
rounded by  a  zone  of  choroidal  atrophy. 

(jjj)  Descending  Neuritis  or  Neui-o- retinitis. — It  is  not  often  pos- 
sible to  distinguish  during  life  between  neuro-retinitis  and  the  slighter 
decrees  of  eno-orored   disk.     In  neuro-retinitis  there  is  only  a  slight 

r5  c      o  111 

deo-ree  of  swellincr,   the  changes  are  more  marked   towards  the  edge 
than  in  the  centre  of  the  disk,  hemorrhages  are  absent,  white  spots 


278  DISORDERS    OF    CRANIAL    XERYES. 

may  be  seen  scattered  over  the  disk  or  along  the  edges  of  the  vessels, 
and  the  disk  has  a  striated  appearance  from  atrophy  of  the  nerve  fibres. 

(iv)  Retrobulbar  Neuritis  and  Perineuritis. — In  retrobulbar  neu- 
ritis the  primary  congestion  soon  passes  on  to  atrophy  with  narrowed 
vessels.  It  is  met  with  in  periostitis  of  the  orbit  and  in  cases  where 
the  optic  nerves  are  constricted  by  thickening  of  the  cranial  bones. 
Optic  perineuritis  results  from  chronic  inflammation  of  the  sheath  of 
the  nerve,  which  gives  rise  to  thickening  and  purulent  infiltration  of 
the  trabeculse,  and  it  generally  ends  in  optic  neuritis. 

(v)  Albuminuric  Retinitis  and  Neuritis. — In  diseases  of  the  kidneys 
the  arteries  of  the  retina  become  diminished  in  calibre  like  the  arterioles 
of  the  body  generally.  As  the  disease  advances  the  retinal  arteries  are 
reduced  to  small  lines,  and  when  swelling  is  present  they  may  be  invisi- 
ble beyond  the  edge  of  the  disk,  while  the  thickening  of  their  walls 
causes  white  lines  to  appear  along  their  edges.  The  arteries  are  liable 
to  undergo  aneurismal  dilatations,  and  retinal  hemorrhages  form  a 
marked  feature  of  the  affection.  Albuminuric  retinitis  ])resents  several 
varieties,  viz.,  (a)  degenerative,  {b)  hemorrhagic,  and  [<■)  inflammatory 
retinitis,  to  which  may  be  added,  according  to  ( Jowers,  {d)  albuminuric 
neuritis. 

(a)  Begenerative  Albuniinurie  Retinitis. — This  form,  which  is  the 
most  common,  begins  by  the  appearance  of  white  spots  on  the  retina; 
they  are  small  and  rounded  at  first,  but  after  a  time  increase  in  size 
and  become  irregular  in  outline,  while  neighboring  spots  sometimes 
coalesce  to  form  large  white  patches.  Small  white  spots  are  generally 
to  be  seen  around  the  macula  lutea;  they  are  sometimes  so  small  as  to 
be  seen  only  on  careful  direct  examination,  but  are  at  other  times  large 
and  well  marked,  and  arranged  end  to  end,  so  as  to  form  ladiating 
streaks  irregularly  disposed  around  the  macula,  and  giving  to  the 
retina  at  this  part  a  silvery  appearance. 

{b)  Hemorrhagic  AJbuminurir  Retinitis. — The  chief  characteristic 
of  this  variety  is  the  large  number  of  hemorrhages  which  occur,  and 
white  spots  only  appear  around  the  macula  lutea  at  a  late  stage  of  the 
affection. 

{c)  Inflammatory  Albuminuric  Retinitis. — In  this  variety  there  is 
general  swelling  of  the  retina,  the  disk  is  obscured,  the  arteries  are 
thready  and  numerous,  the  veins  are  distended  and  tortuous,  with 
irregular  outline,  and  large  hemorrhages  often  occur,  while  the  white 
spots  are  often  numerous  and  well  marked.  On  the  subsidence  of  the 
inflammation  the  optic  nerve  may  undergo  secondary  atrophy. 

[d)  Albumhiuric  Neuritis.~ln  this  affection  inflammation  of  the 
optic  nerve  predominates  over  the  retinal  changes,  the  ed^es  of  the 


DISORDERS    OF    THE    NERVES    OF    SPECIAL    SEXSE.      279 

disk  are  indistinct  and  veiled  under  a  grayish-red  swelling,  and  the 
arteries  are  small  and  often  hidden,  while  even  the  veins  may  be  con- 
cealed in  the  swelling,  and  form  curves  over  the  sides  of  the  swollen 
disk.  White  spots  may  be  seen  on  the  surface  of  the  swollen  disk,  on 
the  retina,  and  around  the  macula  lutea,  and  small  hemorrhages  may 
be  observed  about  the  fundus,  but  are  rare  over  the  swollen  disk. 
When  the  inflammation  subsides  a  consecutive  atrophy  of  the  optic 
nerve  may  be  left.  Albuminuric  neuritis  cannot  often  be  distinguished 
from  ordinary  optic  neuritis. 

General  Symptoms. — Sight  may  remain  unimpaired  in  advanced 
cases  of  optic  neuritis,  and  when  amblyopia  is  present  its  degree  is  by 
no  means  proportional  to  the  amount  of  change  observed  on  ophthal- 
moscopic examination.  Vision  is  likely  to  fail  sooner  in  descendino- 
neuritis  than  in  cases  of  engorged  disk,  while  a  high  degree  of  uni- 
lateral or  bilateral  amblyopia  may  precede  for  some  time  anv  changes 
in  the  fundus  in  retrobulbar  neuritis. 

The  cerebral  symptoms  most  likely  to  be  associated  with  optic  neu- 
ritis are  headache,  vertigo,  vomiting,  loss  of  memory,  unilateral  epi- 
lepsy, hemiplegia,  and  paralysis  of  some  or  all  of  the  ocular  muscles. 

3Iorbid  Anatohiy. — In  order  to  understand  the  mechanism  by  which 
the  swelling  of  the  disk  is  caused  in  optic  neuritis,  the  anatomy  of  the 
nerve  must  be  kept  in  mind.  The  annexed  diagram  (Fig.  86)  will 
suffice  to  remind  the  reader  of  the  structure  of  the  nerve.  Inflamma- 
tion of  the  optic  nerve  gives  rise  to  a  serous  infiltration  which  augments 
its  volume  and  diminishes  its  consistence.  The  sheath  of  the  nerve  is 
often  distended  with  fluid,  the  connective  tissue  of  the  pial  sheath  and 
of  the  trabeculge  surrounding  the  nerve  bundles  becomes  thickened  and 
infiltrated  with  nuclei  and  cells,  a  considerable  number  of  leucocytes  is 
found  surrounding  the  vessels,  and  the  nerve  fibres  undergo  degen- 
erative changes,  while  in  advanced  cases  the  tissue  of  the  lamina 
cribrosa  is  distended  and  its  structure  altered.  The  veins  are  large  and 
tortuous,  but  the  arteries  are  abnormally  small. 

Various  theories  have  been  advanced  to  account  for  the  different  forms 
of  optic  neuritis.  Descending  neuritis  and  perineuritis  of  the  nerve 
are  caused  by  a  local  disease  and  need  not  be  further  discussed.  But 
the  double  optic  neuritis,  or  choked  disk,  which  is  caused  by  the  presence 
of  an  intracranial  tumor  does  not  find  a  ready  explanation.  It  was 
suggested  by  Von  Graefe  that  the  increase  of  intracranial  pressure 
which  results  from  the  presence  of  a  tumor  within  the  skull  caused  an 
obstruction  to  the  flow  of  blood  from  the  eyes  by  compressing  the  cavernous 
sinus.  ]Many  objections  have  been  urged  against  this  theory,  and  it 
was  finally  abandoned  when  Sesemann  showed  that  the  supraorbital  vein 


280 


DISORDERS    OF    CRANIAL    NKRVES. 


anastomoses  so  freely  with  the  f^u-ial  veins,  that  pressure  on  the  cavernous 
sinus  would  only  produce  a  very  temporary  effect.  When  it  was  dis- 
covered l)v  Schwalbe  that  the  subvaginal  space  around  the  oi)tic  nerve 
was  continuous  witli  the  subdural  space  around  the  brain,  Schmidt 
sufTo-ested  that  any  increase  of  intracranial  pressure  would  tend  to  dis- 
tend the  sheath  of  the  optic  nerve  with  fluid,  and  consequently  Avould 
produce  strancrulation  of  the  nerve  fibres  in  tlieir  passage  through  the 
sclerotic  ring  and  Inmin;!  cribrosa.      Tliis  theory  is  by  no  means  free 

Fk;.  86. 


~^^' 


/ 


r'J.HllTiMllltQirlrlAiaiaill'XA. 


inn  A   ti 


/> 


HoHi/.oNTAi,  Section  through  thk  utth  Nkrve  at  its  Point  ok  Insertion  in  thk  »;i,obf,,  anh  it.< 
Passage  through  the  JIembranes  of  the  Eye.  (P'rom  Landois's  "  Ph.vsiologie  "l 
a,  Internal ;  ft,  External  layers  of  the  retina  ;  c,  Choroid  ;  d,  Sclerotic  ;  e.  Physiological  cup ;  f.  Central 
artery  of  the  retina;  </,  Point  of  its  bifurcation  ;  h,  Lamina  crihrosa  ;  7.  Dnral  sheath  ;  m,  sulidural  space  ; 
n,  Suharachnoidal  space  ;  r  Arachnoidal  sheath  ;  j),  Pial  sheatli  :  i  i,  Bundles  of  nerve  tilm-s:  /.  /.,  Connec- 
tive-tissue trabeculaj. 


from  objections.  Optic  neuritis  may  be  absent  in  very  large  tumors 
and  in  chronic  hydroce]:)halus  when  the  increase  of  intracranial  pressui-e 
must  be  very  great,  while  small  cortical  tumors  which  can  scarcely  be 
supposed  to  increase  the  pressure  to  any  appreciable  extent,  often  give 
rise  to  the  most  marked  swelling  of  the  disk.  Dr.  IIuo-hlino;s-.Iackson 
suggested  that  intracranial  tumors  act  like  foreign  bodies,  and  jjroduce 
optic  neuritis  by  their  irritating  effects.  Benedikt  elaborated  this  theory 
still  further.     He  supposed  that  the  irritation  of  the  tumor  acts  on  the 


])TSORI)ERS    OF    THE    NERVES    OF    SPECIAL    SENSE.       281 

Optic  nerves  through  the  vaso-motor  nerves,  and  this  opinion  is  now 
known  as  the  hj])othesis  of  reflex  vaso-motor  action.  In  a  later  pub- 
lication. Dr.  Hughlings-Jackson  maintains  that  the  irritation  of  the 
tumor  causes  a  discharge  from  the  cortex  of  the  1)i-ain,  the  first  result 
of  which  is  to  occasion  spasm  of  the  vessels  of  the  optic  nerves,  which 
is  followed  by  a  secondary  paralysis  of  these,  just  as  occurs  in  voluntary 
muscles  su1)ject  to  unilateral  spasm  from  intracranial  disease.  He 
believes  that  the  nutritive  change  which  constitutes  optic  neuritis  is 
caused  by  this  secondary  paralysis.  I  have  myself  suggested  that  optic 
neuritis  is  a  trophic  change  caused  by  irritation  of  the  external  geniculate 
bodies  which  I  believe  to  be  the  homologues  of  the  spinal  uano-lia. 

(2)  Atrophic  Affkctioxs  of  tue  Optfc  Nervks. 

In  atrophy  of  the  optic  nerve  the  intraocular  extremity  of  the 
nerve  becomes  slowly  and  progressively  transformed  into  a  pure  white, 
or  grayish-Avhite  disk.  There  is  complete  cessation  of  the  capillary 
circulation  of  the  disk  and  consequently  its  healthy  rosy  tint  disappears. 

(a)  Pritnary  Atrophy. — This  form  of  atrophy  is  generally  associated 
with  other  symj)toms  of  locomotor  ataxia,  and  consequently  Charcot 
called  it  tahetlc  amaurosis,  or  parenchyiiiatous  atrophy ;  on  ophthal- 
moscopic examination  the  optic  disk  is  seen  to  be  of  a  pearly  Avhite 
color  (white  atrophy),  occasionally  mixed  with  a  slight  tinge  of  blue  or 
of  gray  (gray  atrophy).  The  contour  of  the  disk  is  sharply  defined, 
and  it  may  maintain  its  normal  size  and  round  form  for  a  long  time, 
although  its  outline  is  occasionally  iri'egular,  and  its  size  reduced.  The 
central  artery  and  vein  maintain  their  normal  volume  and  direction,  but 
the  lateral  branches  of  the  disk  are  in  great  part  atrophied.  White 
atroph\'  is  usually  bilateral,  but  it  may  sometimes  remain  limited  for 
many  years  to  one  eye.  The  retina  is  quite  normal  throughout.  The 
onset  of  the  affection  is  usually  sIoav,  and  the  patient  observes  for  months 
or  years  that  his  sight  is  becoming  progressively  enfeebled.  The  field 
of  vision  becomes  concentricall}-  contracted  but  in  a  very  in-egular 
manner,  and  a  central  scotoma  may  occasionally  be  associated  with  the 
peripheral  limitation.  Dyschromatopsia  or  achromatopsia  is  present  at 
an  early  period  of  the  atrophy,  and  the  acuteness  of  vision  becomes 
progressively  diminished,  but  the  diminution  is  not  always  in  direct 
proportion  to  the  degree  of  change  in  the  optic  nerve,  inasmuch  as  the 
patient  can  sometimes  read  the  smallest  type  when  the  atrophy  is  very 
advanced.  The  patient  may  experience  various  subjective  sensations 
such  as  sparks  or  flashes  of  light  (photopsia),  or  a  play  of  colors  (chro- 
matopsia).  The  mode  of  locomotion  is  characteristic ;  the  head  is 
retracted  and  the  chin  elevated,  the  gait  is  shuflling,  the  eyes  are  directed 


2S'2  DISORDERS    OF    CRANIAL    NERVES. 

upwards,  and  the  expression  of  the  countenance  is  vague  because  the 
eyes  are  not  fixed  on  any  object.  White  atrophy  is  generally  associated 
with  various  disorders  of  the  pupil,  of  which  paralytic  myosis  is  the 
most  fre(|uent.  The  pupillary  disorders  are  independent  of  the  white 
atrophy,  being  caused  by  an  extension  of  the  lesion  which  underlies 
locomotor  ataxia,  to  the  cilio-spinal  region  of  the  cord. 

(b)  Secondary  atmphy  of  the  optic  nerve  is  caused  in  various  ways. 
The  following  varieties  may  be  distinguished  : 

[c)  Atrophy  by  Compression  of  the  Fibres  of  the  Optic  Nerve. — This 
form  may  be  caused  by  pressure  on  the  chiasma  or  on  the  optic  nerve 
in  any  part  of  its  course  through  the  base  of  the  brain,  optic  foramen, 
or  orbit.  It  is  often  preceded  by  a  stage  in  which  the  disk  is  congested, 
but  when  atrophy  is  established  the  ophthalmoscopic  appearances  of  the 
disk  are  the  same  as  those  of  white  atrophy.  A  lesion  of  one  optic 
tract  causes,  but  only  after  some  years,  pallor  of  the  corresponding  halves 
of  the  disk.  The  disease  is  steadily  progressive  and  the  prognosis  is 
most  unfavorable. 

(j)  Atrophy  Secondary  to  Optic  Neuritis. — The  main  features  of 
this  form  of  atrophy  have  already  been  described,  when  the  subsidence  of 
neuritis  was  under  consideration.  The  disk  is  at  first  yelloAv  or  dull 
white,  its  contour  is  completely  hidden  under  an  exudation,  and  the 
vessels  are  varicose ;  but  as  the  exudation  becomes  absorbed  the  disk 
becomes  whiter  and  whiter,  its  capillaries  undergo  atrophy,  and  the 
central  vessels  themselves  become  smaller  although  they  preserve  their 
tortuous  course.  The  disk  is  larger  than  normal,  and  its  edge  is  irregular 
and  broken  and  remains  to  some  extent  obscured  by  exudation,  while 
patches  of  exudation  are  often  seen  around  the  disk  and  in  the  neighbor- 
hood of  the  macula.  This  form  of  atrophy  is  not  always  followed  by 
blindness,  and  patients  after  becoming  blind  during  the  acute  stage  may 
recover  some  degree  of  vision. 

(jj)  Atrophy  Secondary  to  Obliteration  of  Vessels. — This  form  of 
atrophy  is  caused  l)y  embolism  or  thrombosis  of  the  central  artery  of 
the  retina.  The  disk  is  of  a  pearly  white  color ;  its  margin  is  covered 
Avitli  a  Avhite  veil  which  extends  to  the  retina,  and  the  arteries  are  so 
small  as  to  be  scarcely  perceptiljle  and  are  often  surrounded  by  a  whitish 
and  more  or  less  opaque  exudation.  After  the  exudation  has  been 
absorbed  this  form  of  atrophy  is  distinguished  from  every  other  by  the 
small  size  of  the  arteries  of  the  disk  and  retina. 

(jjj)  Choroiditic  Atrophy. — This  form  of  atrophy  is  very  similar  to 
that  which  is  consecutive  to  obliteration  of  the  central  artery  ;  the  retinal 
vessels  are  greatly  atrophied,  but  the  disk  has  a  peculiar  reddish  or 
yellowish  tint  and  its  edges  are  slightlv  blurred. 


I 


\ 


DISORDERS    OF    THE    XERVES    OF    SPECIAL    SENSE.      2«8 

( iv)  Atropliij  Secondary  to  Betinitis  Pigmentom. — In  tins  variety 
of  atroi)hY  the  retinpe  become  studded  by  pio:inentary  spots  from  mitn-a- 
tiou  of  the  choroidal  pigment,  and  the  central  vessels  are  atrophied, 
-while  their  collateral  branches  disappear,  after  a  time,  altogether.  The 
capillary  vessels  derived  from  the  ciliary  arteries  of  the  optic  nerve  are, 
however,  not  affected  to  the  same  extent,  and  consequently  the  disk 
generally  preserves  a  well-marked  rosy  tint. 

( v)  Atrophy  hy  Exravation. — This  optic  atrophy  is  caused  by  increase 
of  intraocular  pressure  in  such  diseases  as  glaucoma  and  hydroi)hthalmia, 
and  it  is  characterized  by  the  deep  excavation  of  the  optic  disk.  A 
certain  degree  of  excavation  may  occur  in  the  other  forms  of  atropliv 
from  wasting  of  the  fibres  of  the  optic  nerve  and  cicatricial  contraction 
of  the  newly  formed  connective  tissue. 

Morbid  Anatomy. — The  anatomical  changes  in  atrophy  of  the  disk 
extend  through  the  optic  nerves.  In  primary  atrophy  the  nerve  is 
much  reduced  in  size ;  it  is  gray  and  gelatinous  in  appearance;  the  con- 
nective-tissue trabeculcTe  are  hypertrophied,  and  the  nerve  fibres  are  pro- 
gressively destroyed,  so  that  the  nerve  is  ultimately  reduced  to  a  cord  of 
connective  tissue.  In  atrophy  from  pressure  the  nerve  is  much  reduced 
in  size  and  the  connective  tissue  is  much  increased.  In  the  various 
forms  of  atrophy  the  disk  presents  a  superficial  depression  which  does 
not  usually  pass  beyond  the  limits  of  the  choroid ;  the  lamina  cribrosa 
is  only  covered  by  a  thin  layer  of  the  debris  of  the  disk,  but  does  not 
itself  undergo  displacement ;  and  the  ganglionic  layer  and  the  nerve 
fibres  of  the  retina  undergo  atrophy,  but  the  other  layers  are  unaffected. 
The  degeneration  always  ascends  to  the  chiasma,  and  the  optic  tracts  are 
atrophied,  in  long-standing  cases,  as  far  as  the  external  geniculate  bodies. 

c.  Diseases  of  the  Optic  Commissure  and  Tracts. 

The  lesions  which  usually  affect  the  optic  tracts  and  commissure  are 
circumscribed  affections  of  the  bones  and  membranes  of  the  brain  or 
injuries  of  the  base  of  the  skull. 

Symptoms. — The  characteristic  symptom  of  disease  of  the  optic  tract 
is  an  enfeeblement  or  abolition  of  sight  of  one  lateral  half  of  the 
retinse.  The  blind  half  of  the  retina  is  separated  from  the  sensitive 
half  by  a  sharply  defined  vertical  line,  but  central  vision  is  preserved 
in  both  eyes.  When  this  condition  is  described  with  reference  to  the 
field  of  vision  it  is  called  hemianopsia,  and  to  the  retina,  hemiopia.  If 
the  left  optic  tract  be  compressed  by  a  tumor  (Fig,  87,  K),  the  two  left 
halves  of  the  retinie — the  outer  of  the  left  and  the  inner  of  the  right — 
are  cut  off  from  the  cortex  and  consequently  there  is  blindness  of  the 


H 


284 


DISORDERS    OF    CRANIAL    NERVES 


ri<'-lit  halves  of  the  fields  of  vision,  a  condition  named  right  lateral 
hcmianopda.  The  affected  portions  of  the  retin;^  are  associated  in  their 
actions,  and  this  condition  has,  therefore,  been  also  named  equilateral 
or  homonymous  hemianopsia.  When  both  the  inner  or  both  the  outer 
halves  of  the  retime  are  blind,  the  condition  is  called  crossed  hemianopsia. 
When  the  lesion  is  situated  over  the  centre  of  tlie  commissure  (Fig. 
ST,  T)  the  inner  halves  of  both  retinae'  are  affected.     AVith  reference  to 

Fig.  87. 


F  THi:  iimir  Tk.vcts.  (After  Charcot. t 
T,  Semidecussation  in  the  cliiasma  ;  TQ,  Decussation  of  fibres  posterior  to  the  external  geiiiciilate  hoUii>ti 
(CG) ;  a' b,  Fibres  which  do  not  decussate  in  the  chiasma;  b' a',  Fibres  coming  from  the  right  eye,  and 
coming  together  in  the  left  hemisphere  (LOG) ;  K,  Lesion  of  the  left  optic  tract  producing  right  lateral 
hemianopsia  ;  A,  Lesion  in  the  left  hemisphere  (LOG),  produces  crossed  amblyopia  (right  eye).  T,  Lesion 
producing  temporal  hemianopsia:  NX,  Lesion  producing  nasal  hemianopsia. 

the  fields  of  vision  this  condition  is  called  double  temporal  hemianopsia. 
In-  this  defect  patients  experience  difficulty  in  walking,  but  they  are 
often  able  to  read  the  smallest  print.  Douhlc  nasal  hemianopsia  is  rare, 
and  can  only  result  from  a  double  lesion  (Fig.  87,  N  N). 


Y.  DISOKDEKS   CAUSED    BY    DISEASE    OF   THE    CEREBRO-SPINAL 
SENSORY   CONDUCTING    PATHS. 

Various  sensory  disorders  are  caused  by  disease  of  the  fibres  of  the 
posterior  roots  after  they  join  the  spinal  cord,  but  inasmuch  as  these  fibres 
are  affected  most  frequently  in  posterior  sclerosis,  the  resulting  dis- 
orders will  be  considered  along  with  tabes  dorsalis. 

Parancesthesia. — In  transverse  lesions  of  the  spinal  cord  the  part 
of  the  body  which  is  innervated  from  that  portion  of  the  cord  which 
lies  below  the  level  of  the  lesion  is  more  or  less  anaesthetic,  according  to 
the  completeness  of  the  destruction  of  the  cord  produced.     A  hyper- 


])ISEASh:    OF    CEREBKO-SFIXAL    SENSORY    PAl'irs.       -iS.") 

iVi^sthetic  belt  is  tiequently  met  Avitli  suirounding  the  body  on  a  level 
Avith  the  iipi)er  limit  of  the  lesion,  caused  by  irritation  of  fibres  descend- 
ing from  the  posterior  roots  which  are  situated  immediately  above  the 
level  of  the  lesion. 

Hejiiiparancesthesia. — In  destructive  lesions  of  one  hiteial  half  (.f 
the  spinal  cord  there  are,  on  the  side  of  the  lesion,  motor  paralysis  and 
loss  of  muscular  sense  below  the  level  of  the  lesion  from  destruction  of 
the  fibres  of  the  pyramidal  tract,  cutaneous  hypemesthesia  of  the  parts 
below  the  level  of  the  lesion  from  irritation  of  the  sensory  conducting 
paths  of  the  opposite  half  of  the  spinal  coitl,  an  anaesthetic  belt  on  a 
level  with  the  lesion  from  implication  of  the  posterior  roots,  and  u  hypcr- 
sesthetic  belt  above  this  level  from  irritation  of  fibres  descending  from 
the  posterior  roots  immediately  above  the  lesion.  On  the  side  opposite 
to  the  lesion   there  is  anaesthesia  of  the  sensations  of  touch,  pain,  tem- 


SeCTION  01'  THE  MeDI  I.LA  OllLliXr.ATA  nX  A  LEVEL  WIT}I  THE  LAEGEST  lHAMETEi;  OF  THE  DISEASED  FOCUS, 
WHICH   IS   KErRESENTED    BV    THE   SHADED    PART   ON   THE   LEFT   HALF   OF   THE   DIA(iRAM.      (After  SENATOR. ) 

P,  pyramids  ;  ol,  olivary  bodies  ;  Voir,  ascending  root  of  tlio  fifth  m-rve ;  A7.-,  nucleus  of  the  vagus ; 
Xiuk,  motor  nucleus  of  the  vagus;  lib,  fasciculus  rotundus ;  x,  the  vagus;  xii,  the  hypoglossal  nerve. 

perature,  and  tickling  of  the  parts  supplied  from  beloAv  the  upper 
limit  of  the  lesion,  from  destruction  of  the  sensory  conducting  ])aths 
after  thev  have  crossed  over  to  the  opposite  side  of  the  cord,  and  a  zone 
of  hypersesthesia  immediately  above  the  level  of  the  upper  limit  of  the 
lesion  caused  by  irritation  of  fibres  descending  from  the  posterior  roots 
immediately  above  the  lesion,  and  some  of  which  jirobably  cross  over  to 
the  diseased  side  of  the  cord.  In  unilateral  lesions  of  the  lumbar  or 
the  cervical  enlargements  a  zone  of  anaesthesia  is  found  in  the  lower 
or  upper  extremities  wdiich  varies  in  its  position  according  to  the  level 
of  the  lesion,  and  the  root  or  roots  which  are  involved  in  it. 


280       DIS<^Kl)EPiS    OF    CEREBRO-SPINAL    SENSOEY    PATHS. 

Crossed  HemianCBstheda. — In  this  affection  there  is  ansesthesia  of 
the  face  on  one  side  of  the  body,  and  of  the  trunk  and  extremities  on 
the  opposite  side.  In  a  case  of  this  kind  reported  bv  Senator  the 
lesion  consisted  of  a  spot  of  softening  in  the  restiform  body,  and  impli- 
cated the  ascending  root  of  the  fifth  nerve  (Fig.  88).  It  must  be  re- 
membered that  this  root  begins  as  low  down  as  the  third  cervical  nerve, 
so  that  some  det^ree  of  anaesthesia  of  the  side  of  the  face  ma}'  be  observed 
in  unilateral  lesions  of  the  upper  portion  of  the  cervical  region  of  the 

cord. 

Hemiancesthesia. — In  this  affection  there  is  loss  of  sensibility  of  the 
whole  of  one-half  of  the  body,  face,  and  extremities,  including  the 
accessible  mucous  membranes  as  well  as  the  skin.  The  abolition  of 
sensation  is  sometimes  incomplete,  and  then  cutaneous  analgesia  or 
thermo-aniesthesia  may  be  present,  while  tactile  sensibility  remains 
unaffected.  At  other  times  the  anaesthesia  of  the  skin  and  mucous 
membranes  is  complete,  and  even  muscular  sensibility  and  muscular 
sense  are  abolished.  The  patient,  for  instance,  does  not  feel  deep  pressure, 
strono-  contraction  of  the  muscles  may  be  produced  by  the  faradic  current 
without  causing  pain,  and  Avhen  his  eyes  are  closed  he  is  unable  to 
describe  the  position  in  which  the  affected  extremities  may  be  placed  by 
passive  movements,  and  is  not  aware  when  his  attemjjted  voluntary 
movements  are  forcibly  prevented.  The  patient  can  walk  Avithout 
difficulty  Avhen  his  eyes  are  closed,  but  by  slight  pressure  upon  the 
affected  side  he  may  be  easily  induced  to  walk  in  a  circle  while  under 
the  impression  that  he  is  walking  in  a  straight  line.  One  hnlf  of  the 
mucous  membrane  of  the  tongue,  mouth,  veil  of  the  palate,  and  the 
conjunctiva  of  the  same  side  are  insensitive,  but  the  cornea  retains  its 
sensibility.  The  affected  side  feels  cold  to  the  touch,  and  the  ])rick 
of  a  pin  does  not  bleed  so  readily  as  on  the  opposite  half  of  the  l)ody. 

The  cutaneous  reflex  actions  may  be  lost  on  the  affected  side  Avhile 
the  deep  reflexes  are  retained. 

The  senses  of  taste  and  smell  are  abolished  on  the  affected  side. 

The  sense  of  hearing  is  diminished,  and  in  some  cases  there  may  be 
complete  unilateral  deafness. 

The  sense  of  sight  is  impaired,  l)ut  not  abolished.  There  is  concen- 
tric restriction  of  the  field  of  vision,  and  the  perception  of  colors  is 
diminished  or  lost  [dgsehronuitopsia),  these  defects  being  present  in  both 
eyes,  but  most  marked  on  the  side  opposite  the  lesion. 

Hemiancesthesia  as  just  described  occurs  in  its  most  typical  form  in 
hysteria  and  occasionally  in  epilepsy,  chorea,  neurasthenia,  and  other 
grave  neuroses.  It  also  occurs  in  organic  diseases  Avhen  the  lesion  is 
situated  in  or  near  the  posterior  third  of  the  posterior  segment  of  the 


DISORDEES    OF    C  EREBE  O  -  SP  I  X  AL    SEXSORY    PATHS.      287 

internal  capsule.  Hemiansesthesia  is  generally  present  in  hemichorea 
and  athetosis,  the  lesion  being  situated  in  these  diseases  either  in  tlie 
external  and  posterior  part  of  the  optic  thalamus  or  in  the  posterior 
part  of  the  lenticular  nucleus.  In  these  diseases  the  posterior  part  of 
the  internal  capsule  is  only  partially  injured  and  the  degree  to  wliich 
sensory  conduction  is  impaired  varies  greatly  in  different  cases.  When 
the  lesion  is  situated  on  the  lenticular  nucleus  the  various  forms  of 
cutaneous  and  muscular  sensibility  are  aifeeted,  but  the  special  senses 
often  remain  intact.  The  special  senses  may  also  remain  unaffected 
Avhen  the  posterior  part  of  the  internal  capsule  is  compressed  bv  the 
growth  of  a  tumor  in  the  optic  thalamus,  probably  because  the  slow 
growth  of  the  tumor  enables  the  fibres  of  the  optic  radiations  of  Gi-atiolet 
to  be  pressed  aside  without  rupture. 

Hystei-ical  hemianfesthesia  is  associated,  as  Ave  have  just  seen,  with 
concentric  restriction  of  the  fields  of  vision  of  both  eyes,  and  especiallv 
with  amblyopia  of  the  eye  on  the  same  side  as  the  other  sensory  dis- 
orders. In  order  to  account  for  this  fact,  Charcot  assumed  that  all  the 
fibres  which  come  from  one  eye  are  connected  with  the  cortex  of  the 
opposite  hemisphere,  and  he  supposed  that  for  the  fibres  w^hich  did  not 
cross  in  the  commissure  there  was  a  suj)plementary  crossing  in  the  corpora 
quadrigemina  (Fig.  87,  T  Q).  But  that  part  of  the  scheme  which  relates 
to  the  supplementary  crossing  is  now,  I  believe,  abandoned  by  its  distin- 
guished author,  because  a  considerable  number  of  cases  are  now  recorded 
in  which  homonymous  lateral  hemianopsia  has  been  caused  by  disease 
of  one  cerebral  hemisphere,  the  lesion  being  situated  in  such  cases  on 
the  pulvinar  of  the  optic  thalamus,  the  white  substance  of  the  occipital 
lobe,  or  the  cortex  of  the  occipital  lobe  as  far  forwards  as  the  angulai- 
gyrus.  From  an  analysis  of  recorded  cases  it  would  appear  that  the 
fibres  of  the  optic  tract  pass  through  the  geniculate  bodies  and  anterior 
tubercle  of  the  corpora  ((uadrigemina,  and  are  continued  upwards  through 
the  pulvinar  of  the  optic  thalamus,  the  posterior  part  of  the  internal 
capsule,  and  the  posterior  part  of  the  corona  radiata,  to  reach  the  cortex 
of  the  occipital  lobe.  In  homonymous  hemianopsia  caused  by  disease 
of  one  optic  tract,  central  vision  is  retained  in  both  eyes,  a  fact  Avhich 
proves  that  the  macula  lutea  of  each  eye  must  be  connected  with  the 
corticles  of  both  hemispheres.  As  the  organs  of  vision  are  bilaterally 
associated  in  their  functions,  it  is  pi-obable  that  the  cortical  visual  centres 
are  connected  by  commissural  fibres  through  the  corpus  callosum. 


288         DISORDERS    OF    CORTICAL    SKXSORY    CENTRES. 


VI.   DISORDERS   CAUSED   BY    DISEASE    OF  THE  CORTICAL 
SENSORY    CENTRES. 

1.  Cutaneous  and  Muscular  1Ie.ml\n.ksthesia. 

Ferricr  localizes  the  centre  of  tactile  sensibility  in  the  hippocanijial 
region,  but  unilateral  lesions  of  these  convolutions  are  not  known  to 
o-ive  rise  to  anesthesia.  Disease  of  the  temporo-sphenoidal  lobe  some- 
times causes  loss  of  tactile  sensibility  of  the  opposite  side,  but  it  is  most 
probably  caused  by  interference  with  the  sensory  fibres  of  the  internal 
capsule.  Cutaneous  aniesthesia  and  loss  of  muscular  sense  have  occa- 
sionally been  found  associated  with  hemiplegia  in  cases  of  extensive 
softening  of  the  cortex  of  the  parietal  lobe,  and  it  is,  therefore,  probable 
that  the  cortical  centre  of  general  sensil»ility  is  widely  diffused  over  the 
so-called  motor  area  of  the  cortex. 


2.     DlSOUDKKS    OF    THF    SeNSE    OF    S.MKl.L. 

a.  Hnlluritiations  of  Smell. — The  case  of  a  woman  is  reported  by 
Dr.  McLane  Hamilton,  Avho  had  for  nearly  thirty  years  suffered  froih 
occasionally  recurring  e]tile[)tiform  attacks  which  were  always  ushered 
in  by  an  aui-a  of  a  disagreeable  (jdor.  The  patient  died  of  phthisis, 
and  at  the  autopsy  the  pia  mater  was  found  adherent  over  the  right 
uncinate  gyrus  and  adjacent  convolutions,  while  the  subjacent  gray 
matter  was  atrophied  and  in  a  state  of  sclerosis.  The  olfactory  neives 
were  not  involved  in  the  lesion. 

/'.  Anosmia. — FeiTier  found  that  destruction  of  iXw.sahtcuhini  cornu 
amnionis  in  monkeys  caused  loss  of  smell  on  the  side  of  the  injury. 
but  in  heiJiiancesthcsio  from  disease  of  the  fibres  of  the  posteri<»r  part  of 
the  internal  capsule  the  loss  of  smell  is  on  the  side  opposite  the  lesion. 
Anosmia  of  the  left  nostril  is  S(»metimes  met  Avith  in  cases  of  right 
hemiplegia  and  aphasia,  but  the  loss  of  smell  is  most  probably  caused 
by  softening  of  the  external  root  of  the  olfactory  tract  and  not  from 
disease  of  the  cortex.  A  case  of  abscess  of  the  temporo-sphenoidal 
lobe  is  reported  by  Dr.  Glynn,  in  which  the  most  prominent  symptom 
was  complete  anosmia,  l)ut  the  loss  of  smell  was  most  prol)ably  caused 
by  compression  of  the  olfactory  tracts  at  their  points  of  junction  with 
the  brain.  On  the  whole,  our  clinical  information  with  regard  to  the 
localization  of  the  cortical  centre  of  smell  is  exceedingly  scanty  and 
will  not  bear  a  critical  investio;ation. 


I 


DISEASES    OF    THE    COKTICAL    SEXSOKY    CEXTEES.      289 


•S.  Disorders  of  the  Auditory  Sense. 

a.  Hallucinations. — Ferrier  places  the  auditory  cortical  centre  in 
the  first  and  second  convolutions  of  the  temporo-sphenoidal  lobe,  and 
irritative  lesions  of  these  convolutions  give  rise  occasionally  to  hallucina- 
tions of  hearing.  A  man,  under  my  care,  received  a  blow  over  the 
head  a  little  above  the  left  ear,  and  at  the  seat  of  injury,  which  was 
opposite  the  first  and  second  temporo-sphenoidal  convolutions,  a  slight 
depression  in  the  bone  could  be  detected.  After  the  injury  the  patient 
suffered  from  recurring  epileptiform  attacks  which  were  ushered  in  by 
loud  rattling  noises,  caused  most  probably  by  a  discharging  lesion  havin^ 
its  origin  in  the  auditory  cortical  centre. 

h.  Psyehical  Deafness. — In  this  condition,  which  was  first  described 
by  Goltz  as  occurring  in  dogs  after  portions  of  the  cortex  of  the  brain 
had  been  washed  away,  the  animal  is  not  deaf,  but  fails  to  recognize 
the  significance  of  the  usual  calls.  He  does  not,  for  example,  respond 
to  the  call  of  his  name,  and  is  not  cowed  by  angry  threats,  and  yet 
distinct  evidence  is  obtained  that  he  hears  noises.  This  defect  was 
named  psychical  deafness  by  Munk.  The  state  in  man  most  nearly 
approaching  to  it  is  word-deafness.,  which  will  be  subsequently  described 
along  with  the  disorders  of  speech. 

c.  Absolute  Deafness. — Unilateral  destructive  lesions  of  the  first 
and  second  temporo-sphenoidal  convolutions  do  not  give  rise  to  complete 
deafness  of  one  ear,  because  the  sense  of  hearing  is  bilaterally  associated, 
and  so  long  as  one  hemisphere  is  unaffected  the  auditory  sense  remains 
unimpairevl  or  only  slightly  weakened.  The  condition  which  will  be 
subsequently  described  as  word-deafness  is,  however,  associated  with 
disease  of  the  first  and  a  portion  of  the  second  temporo-sphenoidal  con- 
volutions. But  if  the  first  and  second  tem})oro-si)henoidal  convolutions 
contain  the  auditory  centres,  bilateral  lesions  of  these  ought  to  give  rise 
to  complete  deafness.  A  case  is  reported  by  Wernicke  in  which  the 
patient  first  suffered  from  word-deafness  and  subsequently  became  com- 
pletely deaf,  and  after  death  the  first  temporo-splienoidal  convolution 
was  found  softened  in  each  hemisphere.  A  careful  dissection  of  the 
ears  proved  the  absence  of  any  local  disease  of  the  peripheral  organ  of 
hearing. 

4.  Disorders  of  the  Visual  Sense. 

a.  Halluei7iations  of  Sight. — Tumors  of  the  occipital  lobe  give  rise 
to  hallucinations  of  sight  such  as  colored  vision,  and  the  images  of  animals 
and  of  variously  dressed  men,  and  when  the  growth  causes  epileptiform 
convulsions  the  attacks  are  often  preceded  by  a  visual  aura. 

19 


290  DISORDEES    OF    THE    VISUAL    SENSE. 

b.  Psychical  Blindness.— Ti\\&  condition  was,  like  psychical  deafness, 
first  observed  by  Goltz  in  dogs  after  portions  of  the  cortex  of  the  brain 
were  washed  away.  The  dog,  after  the  operation,  sees  and  avoids 
obstacles,  thus  recognizing  resistance  and  the  other  fundamental  prop- 
erties of  matter,  but  he  has  lost  the  power  of  appreciating  the  special 
properties  of  matter  to  so  great  an  extent  that  he  does  not  recognize  his 
food  as  such.  A  more  or  less  similar  condition  has  been  descril:)ed  hx 
Fiirstner  as  occurring  in  some  cases  of  general  paralysis  of  the  insane. 

The  patient,  for  example,  recognizes  that  a  piece  of  money  placed  in 
his  hand  is  a  metal,  but  has  lost  all  knowledge  of  the  special  properties 
which  constitute  it  a  coin.  Word-blindness  is  a  more  or  less  similar 
condition.  Subsequent  dissection  has  proved  that  in  the  dogs  operated 
upon  by  Goltz,  it  was  the  posterior  lobes  of  the  brain  which  were  chiefly 
denuded  of  cortex  by  his  method  of  procedure,  and  in  Fiirstner"s  cases 
the  cortex  of  the  occipital  lobes  was  always  found  diseased  when  a 
post-mortem  was  obtained.  It  will  be  hereafter  seen  that  in  word-blind- 
ness the  disease  is  limited  mainly  to  the  cortex  of  the  angular  gyrus. 

c.  Homonymous  Bilatcnd  Hemianopsia. — Man^^  cases  are  now  re- 
corded in  which  this  defect  of  sight  was  caused  by  softening  of  the  cortex 
of  the  left  angular  gyrus,  and  the  condition  is  frequently  associated  with 
word-blindness. 

d.  Absolute  Blindness. — Disease  of  the  cortex  of  one  hemisphere 
of  the  brain  does  not  usually  give  rise  to  complete  blindness.  The  case 
of  a  boy,  however,  is  reported  by  Dr.  Abercombie,  who,  after  an  injury 
which  caused  a  depressed  fracture  of  the  right  parietal  bone,  suftered 
from  hemiplegia  of  the  left  side  and  amaurosis  of  the  left  eye,  from 
which  he  made  a  quick  recovery  on  the  depressed  part  being  removed. 
The  position  of  the  fracture  rendered  it  probal)le  that  the  angular  gyrus 
was  injured.  A  case  is  reported  by  Dr.  Glynn,  of  Liverpool,  in  which 
the  patient  became  suddenly  and  completely  blind,  and  in  which  a  clot 
was  found  occluding  the  posterior  cerebral  artery  of  the  left  side,  causing 
extensive  softening  of  the  left  occipital  and  temporo-si)henoidal  lobes. 
The  case  of  a  woman  is  reported  by  Dr.  Shaw,  of  Brooklyn,  who  had 
become  suddenly  aphasic  and  perfectly  deaf  and  blind.  At  the  autopsy 
the  angular  gyri  and  superior  temporo-sphenoidal  convolutions  of  both 
hemispheres  were  found  completely  atrophied,  and  no  other  lesions  could 
be  discovered  in  the  brain  or  peripheral  organs.  This  case  Avould  seem 
to  indicate  that  bilateral  disease  of  the  angular  gyri  will  alone  suffice  to 
cause  complete  blindness.  Berger  has  recently  recorded  two  cases  of 
complete  blindness  with  normal  or  almost  normal  reaction  to  light  of 
the  pupils  and  in  which  extensive  softening  was  found  in  the  occipital 
lobes. 


DISEASES    OF    THE    CORTICAL    SEXSOEY    CENTRES.       291 

Nothing  is  known  of  disorders  of  the  sense  of  taste  from  cortical 
disease. 

Treatment. — Inasmuch  as  anaesthesia  and  hyperjesthesia  are  generally 
associated  with  other  important  phenomena  such  as  motor  paralysis,  the 
treatment  of  these  symptoms  does  not  require  to  be  specially  cfiscussed 
in  this  place.  In  the  treatment  of  neuralgia  the  first  indication  is  to 
remove  the  exciting  cause.  An  endeavor  must  be  made  to  remove  every 
source  of  external  irritation  such  as  carious  teeth,  foreign  bodies  pressino- 
upon  the  nerves,  cicatrices,  tumors,  and  neuromata.  It  is  manifest  that 
in  order  to  fulfil  this  indication  great  scope  is  afforded  the  exercise  of 
surgical  skill.  At  other  times  the  exciting  cause  of  a  neuralgia  is  to 
be  found  in  remote  irritation  such  as  when  the  presence  of  intestinal 
worms  or  uterine  disease  gives  rise  to  facial  neuralgia.  Venous  conges- 
tion of  the  pelvic  organs  from  constipation  and  portal  obstruction  is 
sometimes  the  cause  of  sciatica,  and  in  these  cases  benefit  is  likely  to  be 
obtained  from  purgatives  and  the  use  of  natural  saline  waters  like  those 
of  Kissingen,  Marienbad,  and  Harrogate.  A  turpentine  enema  has 
also  been  strongly  recommended  in  such  cases.  The  early  stages  of 
neuralgia  which  arises  in  rheumatic  and  gouty  subjects  must  be  treated 
by  absolute  rest,  diaphoresis,  the  milder  counter-irritants,  the  vapor  or 
Turkish  bath,  and  salicylate  of  soda  or  alkalies  with  colchicum,  and  by 
iodide  of  potassium  either  alone  or  in  combination  with  guaiacum,  when 
the  acute  symptoms  have  subsided.  When  the  patient  is  suffering  from 
anpemia,  as  often  occurs  in  trigeminal  neuralgia,  large  doses  of  carbonate 
of  iron,  with  or  without  cod-liver  oil,  have  a  very  beneficial  effect.  In 
such  cases  arsenic  either  alone  or  combined  with  iron  is  a  useful  remedy, 
and  it  is  also  useful  in  ophthalmic  neuralgia  of  malarial  origin.  In 
malarial  neuralgia,  however,  large  and  repeated  doses  of  quinine  are  the 
most  trustworthy  remedy  and  it  also  may  be  employed  in  the  treatment 
of  other  forms  of  neuralgia,  and  is  especially  useful  in  trigeminal 
neuralgia.  In  neuralgia  of  syphilitic  origin  large  doses  of  iodide  of 
potassium  must  be  given,  and  this  drug  will  also  be  useful  whenever  there 
is  reason  to  suspect  the  presence  of  neuritis.  Zinc,  nitrate  of  silver, 
chloride  of  gold  and  sodium,  and  strychnia,  are  other  drugs  which  have 
occasionally  been  found  useful  in  the  treatment  of  neuralgia.  Gelse- 
minum  sempervirens,  best  given  in  the  form  of  tincture,  and  croton 
chloral  hydrate,  either  in  one  large  dose  of  a  scruple  or  in  four  grain 
doses  every  four  hours,  have  been  found  useful  in  the  treatment  of 
trigeminal  neuralgia,  and  Dr.  Ringer  speaks  favorably  of  a  liquid  extract 
of  tonga  prepared  by  Messrs.  Allen  k  Handbnry,  given  in  drachm 
doses  every  four  hours.  In  sciatica,  rectified  oil  of  turpentine  has 
been  found  useful.     It  is  best  administered  in  gelatine  capsules  each  of 


292  TKEATMENT. 

which  contains  fifteen  drops  of  the  oil,  and  two  or  three  of  these  may 
be  given  at  meal-time.  Copaiba  has  succeeded  in  the  hands  of  Dr. 
March,  of  Rochdale.  The  local  treatment  of  neuralgia  consists  of  the 
application  of  hot  fomentations  and  poultices  in  the  early  stages,  while 
flying  blisters  may  be  applied  along  the  course  of  the  painful  nerve 
when  the  acute  symptoms  have  subsided.  When  the  nerve  is  deep-' 
seated  like  the  sciatic  its  course  may  be  painted  Avith  tincture  of  iodine, 
or  the  actual  cautery  may  be  used  in  chronic  and  obstinate  cases.  In 
such  cases  a  very  effectual  but  very  severe  remedy  consists  in  the  sub- 
cutaneous injection  over  the  seat  of  severest  pain  of  a  few  minims  of  a 
strong  solution  of  nitrate  of  silver  (gr.  x  to  5j)-  An  injection,  by 
means  of  a  subcutaneous  syringe,  into  the  substance  of  tlie  nerve  of  a 
one  per  cent,  solution  of  perosmic  acid  has  been  favorably  reported  upon 
by  Eulenburg  and  others.  Ointments  containing  opium,  veratria, 
aconitia,  or  equal  parts  of  chloral  and  camphor,  may  be  rubbed  into  the 
skin  over  the  painful  nerve,  or  the  course  of  the  nerve  may  be  painted 
with  aconite  or  belladonna  liniment,  or  rubbed  with  narcotic  and  sooth- 
ing liniments.  Chloroform  is  also  found  useful  as  a  local  application, 
and  its  inhalation  may  be  advisable  to  allay  the  pain  of  very  violent 
paroxysms  of  neuralgia.  Chloral  and  camphor  when  rubbed  together 
in  a  mortar  form  a  clear  solution  Avliich  is  an  excellent  local  application 
in  neuralgia  of  superficial  nerves. 

The  constant  current  has  been  found  very  successful  in  the  treatment 
of  obstinate  neuralgia.  /In  neuralgia  of  isolated  superficial  branches 
the  direction  method  may  be  employed  and  a  descending  stahilr  current 
passed  through  the  painful  nerve.  AYhen  the  polar  method  is  used,  the 
anode  is  to  be  placed  on  the  specially  painful  points  and  held  stationary 
there,  whilst  the  cathode  rests  on  the  back  of  the  neck,  sternum,  or  on 
any  other  indifferent  part  of  the  body.  When  the  deeper-seated  nerves 
are  affected,  the  anode  may  be  placed  on  some  indifferent  part  of  the 
body  and  the  cathode  over  the  point  of  emei'gence  of  the  affected  nerve. 
In  order  to  reach  the  main  divisions  of  the  fifth  nerve  at  the  base  of 
the  cranium,  and  after  their  emergence  through  the  foramen  of  the 
sphenoid  bone,  the  current  may  be  conducted  transversely  through  the 
base  of  the  skull  at  the  appropriate  spots,  the  anode  being  placed  on  the 
painful  side.  /Benedict  recommends  that  in  severe  cases  of  trigeminal 
neuralgia  galvanic  currents  should  be  passed  longitudinally  and  trans- 
versely through  the  skull,  and  along  the  sympathetic  nerve.  Faradiza- 
tion occasionally  answers  better  than  the  constant  current,  the  moist 
poles  being  applied  to  the  painful  points  and  along  the  nerve  trunks. 
The  electric  hand  is  sometimes  very  soothing  and  agreeable  to  the 
patient. 


DISEASES    OF    THE    CORTICAL    SENSORY    CENTRES.       293 

In  the  treatment  of  sciatica  the  anode  should  be  placed  over  the  sciatic 
foramen  or  upon  the  sacrum,  and  the  cathode  upon  the  specially  painful 
parts.  Remak  advises  that  successive  portions  of  the  nerve,  from  six 
to  eight  inches  in  length,  should  be  successively  brought  under  the 
influence  of  tlie  current,  beginning  at  the  sacrum  and  passing  down  to 
the  feet.  Another  method  recommended  by  Remak,  under  the  name 
of  circular  current,  consists  in  the  stabile  application  of  the  anode  upon 
the  painful  points  and  over  the  trunk  of  the  nerve;  broad  electrodes 
and  strong  currents  being  used.  In  severe  cases  Benedict  recommends 
that  one  electrode  should  be  introduced  into  the  rectum  and  the  other 
placed  over  the  sacrum,  so  that  the  current  may  pass  through  the 
plexus.  Ciniselli  recommended  a  zinc  and  copper  plate  connected  by 
a  wire,  to  be  applied  to  the  aifected  limb  and  worn  continuously.  In 
chronic  cases  I  have  obtained  excellent  results  by  introducing  several 
acupuncture  needles  over  the  course  of  the  nerve  as  it  emerges  from  the 
sciatic  foramen,  and  passing  a  feeble  galvanic  current  through  them, 
the  positive  pole  being  in  contact  with  the  needles  and  the  negative 
placed  over  the  sacrum.  (The  faradic  current  gives  the  best  results 
when  the  pain  has  in  great  measure  disappeared  and  the  subsequent 
muscular  feebleness  has  to  be  treated,  or  if  more  or  less  antesthesia  be 
present  the  faradic  brush  may  be  employed. 

(tnoi'dpr  to  nft'nrd  immediate  relief  to  the  pain  the  administration  of 
narcotics  forms  an  indispensable  part  of  treatment.  The  most  generally 
effectual  narcotic  is  morphia  administered  by  subcutaneous  injection. 
Another  useful  method  of  employing  morphia  is  to  dust  from  one-sixth 
to  one-third  of  a  grain  every  three  or  four  hours  over  the  raw  surface 
left  when  the  cuticle  is  removed  by  the  application  of  a  blister  over  the 
course  of  the  painful  nerve.  It  may  also  be  useful  to  change  some- 
times from  morphia  to  stramonium,  hyoscyamus,  or  atropine.  In 
the  treatment  of  epileptiform  trigeminal  neuralgia  Trousseau  recom- 
mended the  use  of  large  doses  of  opium  or  morphia,  and  in  some  cases 
he  prescribed  as  much  as  a  drachm  of  morphia,  or  two  or  three  of 
opium  in  the  course  of  the  day ;  but  this  treatment  ought  only  to  be 
resorted  to  -when  every  other  method  fills.  Large  doses  of  bromide  of 
potassium,  either  alone  or  in  combination  with  tincture  of  opium  or 
chloral,  act  beneficially  sometimes  in  this  form  of  neuralgia.  In  intrac- 
table cases  of  neuralgia  relief  for  the  pain,  when  all  other  methods  fail, 
is  only  to  be  obtained  by  means  of  surgical  operations.  Resection  of  the 
painful  nerve,  and  even  amputation  of  the  affected  limb,  have  been  resorted 
to  in  intractable  cases,  but  such  serious  operations  ought  only  to  be 
resorted  to  under  the  most  pressing  necessity.  Stretching  of  the  affected 
nerve  is  a  much  less  serious  operation,  and  several  cases  of  neuralgia 


294  TREATMENT. 

of  different  nerves  are  now  on  record  in  which  the  operation  has  proved 
successful.  Lange  procured  relief  of  pain  in  sciatica  by  producing 
forcible  flexion  of  the  thigh,  and  thus  stretching  the  affected  nerve 
over  the  neck  of  the  femur. 

The  form  of  plantar  neuralgia  described  by  S.  Weir  Mitchell  has 
hitherto  proved  intractable  to  every  kind  of  treatment.  The  posterior 
tibial  nerve  was  stretched  in  one  of  ray  patients  by  my  colleague, 
Mr.  Southam,  but  the  relief  which  followed  was  not  lasting. 

Coccygodynia,  in  addition  to  the  usual  remedies,  must  sometimes 
be  treated  by  means  of  a  surgical  operation.  The  usual  operations  are 
extirpation  of  the  coccyx,  and  separation  of  the  bone  from  all  the  nerves 
connected  with  it  by  means  of  a  tenotomy-knife  introduced  subcu- 
taneously. 

Disorders  of  the  special  senses  come  under  the  care  of  the  physician 
as  symptoms  of  other  diseases  of  the  nervous  system,  and  the  treatment 
must  be  directed  against  the  chief  lesion,  whatever  it  may  be.  'I'he 
possibility  of  the  sensory  affection  being  of  syphilitic  origin  should 
never  be  forgotten.  Local  electrical  treatment  is  sometimes  found 
useful  in  those  cases  in  which  the  acuteness  of  any  of  the  special  senses 
is  diminished. 

The  treatment  of  those  sensory  disorders  which  are  caused  by  disease 
of  the  sensory  conducting  paths  and  cortical  centres,  must  vary  accord- 
ing to  the  nature  and  locality  of  the  lesion.  Local  treatment  is  seldom 
of  any  use. 


CHAPTER    III. 

SPASMODIC  DISORDERS. 

The  general  characteristics  of  the  various  forms  of  spasm  have  ah-eady 
been  considered  and  we  shall  now  describe  in  detail  (I.)  the  spasms 
which  are  caused  by  reflex  or  direct  irritation  of  the  reflex  spinal 
mechanisms  and  which  may  be  named  spino-neural  spasms,  and  (II.)  the 
spasms  which  are  caused  by  irritation  of  the  cortical  motor  centres  or 
of  the  fibres  of  the  pyramidal  tracts,  and  which  may  be  named  cereljro- 
spinal  spasms.  It  is  not  always  possible  to  make  a  trenchant  division 
between  these  two  forms  of  spasm.  Some  fornas  of  writer's  cramp,  for 
instance,  belong  probably  to  the  spino-neural,  and  others  to  the  cerebro- 
spinal paralyses,  and  even  some  local  spasms  like  masticatory  spasm 
may  be  caused  either  by  reflex  irritation  or  by  irritation  of  the  cortex 
of  the  brain,  but  it  will  be  found  convenient  to  describe  all  forms  of 
these  affections  in  the  same  place.  Notwithstanding  the  difficulties 
which  present  themselves  in  carrying  out  this  division  of  spasm,  the  im- 
portance of  the  distinction  Avliich  underlies  the  classification  must  be  our 
justification  for  adopting  it. 

I.  SPINO-NEURAL   SPASMS. 

The  spino-neural  spasms  may  be  divided  into :  1,  local  spasms  affect- 
ing muscles  supplied  by  particular  nerves  or  their  branches  ;  2,  general 
spasms  caused  by  excessive  irritability  of  the  spinal  reflex  mechanisms  ; 
and  3,  spasms  of  myopathic  origin.  Amongst  the  spino-neural  spasms 
tetanus  and  tetany  are  here  included,  but  we  are  by  no  means  sure  that 
a  more  extended  knowledge  of  the  pathology  of  these  affections  will 
justify  their  retention  in  this  category. 

1.  Local  Spasms. 
a.  Spasms  of  the  3Iuscles  of  the  Eyeball. 

The  external  muscles  of  the  eyeballs  are  subject  to  both  tonic  an<l 
clonic  spasms. 

(1)  Tonic  spasm  of  the  internal  rectus  is  more  frequent  than  spasm 
of  any  other  muscle  of  the  eyeball,  and  it  is  usually  associateil  with 


296  SPASMODIC    DISORDERS. 

blepharospasm.  It  gives  rise  to  homonymous  diplopia  similar  to  that 
which  occurs  in  paralysis  of  the  sixth  nerve,  but  in  the  latter  the  squint 
is  permanent  and  the  relative  positions  of  the  true  and  false  images 
fixed,  while  in  the  former  there  is  a  constant  oscillation  between  the  two 
images  which  alternately  approach  and  recede  from  each  other.  All 
easel  of  spasmodic  strabismus  are  accompanied  by  paroxysms  of  neuralgia, 
and  by  photophobia  and  lachrymation.  Tonic  spasm  of  the  internal 
rectus  may  be  caused  by  long-standing  paralysis  of  the  external  rectus. 

(2)  Tonic  sjjasm  of  the  external  rectm,  which  is  rare,  causes  diver- 
gent squint,  and  gives  rise  to  diplopia  with  crossed  images,  but  contrary 
to  what  occurs  in  paralysis  the  two  images  never  remain  fixed,  but 
alternately  approach  and  recede  from  each  other. 

(3)  Nystagmus  consists  of  a  clonic  spasm  of  the  muscles  of  both 
eyeballs,  giving  rise  to  continual  lateral  oscillatory  or  rotatory  move- 
ments which  are  entirely  beyond  the  control  of  the  patient.  When  the 
patient  looks  at  a  remote  object  the  trembling  liecomes  very  pronounced, 
but  the  eyes  become  more  and  more  fixed  in  proportion  as  they  are 
directed  to  near  or  small  objects.  Nystagmus  may  be  caused  by  con- 
genital cataract,  corneal  opacities,  and  other  local  diseases,  but  it  is  ver}'^ 
generally  due  to  central  changes  and  is  a  prominent  symptom  in  sclerosis 
in  patches,  and  in  Friedreich's  hereditary  form  of  locomotor  ataxia, 
while  it  may  arise  in  connection  with  meningitis,  hydrocephalus,  and 
other  intracranial  diseases.  It  is  often  present  in  albinos,  and  colliei's 
are  frequently  affected. 

h.  Masticatory  Spasm  {Trismus). 

Etiology. — Bilateral  masticatory  spasm  is  often  a  symptom  of  general 
spasms,  such  as  tetanus,  epilepsy,  hysteria,  and  chorea.  When  it  occurs 
as  a  separate  affection  it  may  be  caused  by  disease  of  tlie  motor  nerves 
themselves,  or  be  a  symptom  of  basal  meningitis,  apoplexy,  intracranial 
tumors,  and  other  central  diseases.  It  may  also  result  from  reflex 
irritation  either  of  the  sensory  branches  of  tiie  fifth  nerve  or  of  some 
remote  part  of  the  body. 

Symptoms. — The  spasm  is  generally  bilateral  and  it  may  be  either 
tonic  or  clonic. 

In  the  tonic  variety  the  lower  is  approximated  to  the  upper  jaw,  and 
when  the  teeth  are  so  firmly  clenched  that  they  cannot  be  separated  from 
one  another  by  force  the  condition  is  named  lock-jaws  or  trismus.  The 
muscles  of  the  jaw  are  then  tense,  rigid,  often  painful,  and  mastication 
is  impossible.  In  the  clonic  variety  the  lower  jaw  is  moved  either  in  a 
vertical  or  horizontal  direction,  the  former  giving  rise  to  chattering  of 


SPIXO-NEURAL    SPASMS.  9i)7 

the  teeth,  as  in  the  cohl  stage  of  ague,  and  the  hitter  to  grinding  and 
munching  of  the  teeth.  The  teeth  are  much  ^vorn  hy  the  constant 
grinding  against  each  other,  and  they  may  even  be  broken  l)y  the  vio- 
lence of  the  spasm. 

c.  Spasm  in  the  Area  of  Distribution  of  the  Facial  Nerves  (Histrionic 
Spasm,  Mimic  Convulsion,  Convulsive  Tic). 

Etiologij. — Convulsive  tic  sometimes  appears  to  be  inherited,  and  it 
may  occur  in  neuroi)athic  subjects  from  emotional  causes,  or  in  tlie 
absence  of  any  recognizalde  cause.  It  is  caused  frequently  by  direct 
or  indirect  irritation  of  the  facial  nerve.  The  direct  causes  are  often 
only  a  slighter  degree  of  those  which  occasion  paralysis  of  the  nerve, 
such  as  exposure  to  cold,  tumor  of  the  base  of  the  brain  or  in  the 
lower  end  of  the  pons,  aneurism  of  the  vertebral  artery,  inflamed 
glands  in  the  neighborhood  of  the  stylo-mastoid  foramen,  abscess  of  the 
parotid  gland,  caries  of  the  petrous  portion  of  the  temporal  bone,  and 
otitis.  Reflex  irritation  is  often  conveyed  through  the  fifth  nerve  and 
the  causes  of  irritation  are  trigeminal  neuralgia,  carious  teeth,  an<l  irri- 
tation of  the  eyeball  and  conjunctiva.  The  source  of  irritation  is, 
however,  sometimes  remote,  the  spasm  having  been  caused  by  such 
diseases  as  cervico-brachial  neuritis,  and  intestinal  or  uterine  disease. 

Symptoms. — Facial  spasm  may  be  clonic  or  tonic,  the  former  being 
by  far  the  more  frequent. 

The  clonic  form  is  characterized  by  periodically  recurring  attacks  of 
spasm,  each  paroxysm  consisting  of  sudden  and  violent  contractions 
and  relaxations  of  some  of  the  muscles  of  the  face.  The  duration  of 
each  paroxysm  varies  from  a  few  seconds  to  a  few  minutes,  and  the 
interval  between  them  is  generally  brief,  except  during  sleep,  when  the 
spasms  entirely  cease.  The  spasm  is  generally  unilateral,  and  thus 
the  contortions  and  grimaces  of  the  affected  side  contrast  strangely 
with  the  calm  expression  of  the  healthy  side.  The  contortions  pro- 
duced are  extremely  varial)le  and  consist  mainly  of  elevation  and 
depression  of  the  occipital  and  frontal  muscles,  corrugation  of  the  eye- 
brows, twitching  or  winking  of  the  eyelids,  elevation  of  the  cheek  and 
of  the  nostril,  and  distortion  of  the  angle  of  the  mouth,  these  symp- 
toms being  present  either  singly  or  in  every  imaginable  combination. 
The  spasm  is  sometimes  partial,  being  limited  to  the  muscles  supplied 
by  single  branches  of  the  nerve.  The  palpebral  twigs  alone  are  some- 
times affected,  and  the  spasm  then  manifests  itself  by  a  rapid  winking 
called  nictitating  spasm.  In  some  cases  there  is  only  slight  twitching 
movements  of  one  of  the  eyelids,  the  lower  being  the  one  uiost  usually 


298  SPASMODIC    DISORDERS. 

affected.  At  other  times  the  spasm  gives  rise  to  a  paroxysmal  closure 
of  the  evelids  which  may  last  from  a  few  minutes  to  a  feAv  hours,  and 
mav  occasionally  extend  over  a  period  of  weeks  or  months,  this  form 
beiiag  named  blepharospasm.  This  form  is  accompanied  by  photo- 
phobia, and  is  generally  caused  by  reflex  irritation  of  the  fifth  nerve. 
In  some  other  cases  the  spasm  is  limited  to  the  area  of  distribution  of 
the  malar  and  labial  branches,  and  then  it  gives  rise  to  a  convulsive 
orin  on  one  or  both  sides,  resembling  laughing,  and  consequently  this 
form  is  called  the  sardonic  laugh,  risus  eaninus,  or  ct/nic  spasm.  All 
the  muscles  supplied  by  the  fecial  nerve,  including  the  platysma 
myoides,  may  be  involved,  and  the  spasm  sometimes  extends  to  the 
territories  of  other  nerves,  such  as  the  fifth,  hypoglossal,  spinal  acces- 
sory, and  upper  branches  of  the  brachial  plexus. 

Sensory  disorders  never  form  a  prominent  feature  of  the  disease, 
but  the  patient  may  occasionally  suffer  from  numbness  or  even  a  slight 
deuree  of  pain  in  the  side  of  the  face,  and  he  may  also  complain  of 
headache  and  tinnitus  aurium.  Vaso-motor  and  secretory  disorders 
are  never  present,  the  electrical  reactions  of  the  affected  muscles  are 
normal,  and  all  the  voluntary  movements  of  the  face  can  be  executed 
with  undiminished  power.  Certain  points  may  be  discovered,  pressure 
on  which  will  arrest  the  spasm  ;  these,  when  present,  correspond  with 
the  pressure  point  in  trigeminal  neuralgia. 

The  tonic  form  of  facial  spasm  was  first  clearly  recognized  by  Dr. 
Marshall  Hall.  In  this  form  the  muscular  contraction  is  persistent, 
the  tip  of  the  nose,  the  angle  of  the  mouth,  and  the  chin  are  drawn  to 
the  affected  side,  and  the  furrows  and  dimples  of  that  side  are  rendered 
deeper.  The  contracted  muscles  render  the  tissues  too  scanty  for  cov- 
ering the  orifices,  so  that  when  the  eye  is  closed  a  tightness  is  induced 
at  the  angle  of  the  mouth,  and  when  the  angle  of  the  mouth  is  moved 
further  from  the. eye,  as  in  speaking,  it  is  difficult  to  keep  the  eye  closed, 
articulation  is  rendered  indistinct,  and  tlie  bolus  of  food  tends  to  collect 
between  the  teeth  and  the  affected  cheek,  causing  slight  trouble  during 
mastication,  but  there  is  no  difiiculty  of  deglutition. 

d.  Spasm  of  the  3Iuscles  Supplied  hy  the  Hypoglossal  Kerve 
{Lingual  Spasm,  Aphthongia). 

Etiology. — Lingual  spasm  is  rare  as  an  independent  affection,  but  is 
a  common  symptom  of  hysteria,  chorea,  epilepsy,  and  eclampsia,  while 
it  often  accompanies  spasm  of  the  muscles  supplied  by  the  fifth  nerve. 
Spasm  of  the  tongue  may  also  result  from  meningitis,  and  lesions  of  its 
cortical  motor  centre,  and  it  is  frequently  met  with  in  bilateral  athetosis 


SPINO -NEURAL    SPASMS.  299 

and  the  spasmodic  paralyses  of  infancy,  while  tremor  of  the  tono-ue  is  a 
symptom  of  progressive  bulbar  paralysis,  and  disseminated  sclerosis. 

Symptoms. — In  lingual  spasm  the  muscles  innervated  by  the  hypo- 
glossal nerve  are  thrown  into  a  state  of  clonic  or  tonic  convulsions 
when  the  patient  attempts  to  speak,  the  affection  being  more  or  less 
similar  to  writer's  cramp,  and  the  spasms  implicating  groups  of  other 
muscles  engaged  in  effecting  special  movements.  In  some  cases  the 
tongue  becomes  fastened  to  the  hard  palate  by  a  tonic  spasm  whenever 
the  patient  tries  to  speak,  but  in  other  cases  it  is  attacked  with  clonic 
spasms,  and  the  sterno-hyoid,  thyro-hyoid,  and  sterno-thyroid  may  like- 
wise be  implicated  in  the  convulsion. 

c.  Spasm  of  the  Muscles  Supplied  hij  the  Vagus  and 
Pharyngeal  Plexus. 

(1)  Spasm  of  the  Soft  Palatk,  Pharynx,  and  (Esophagus. 

('/)  Spasm  of  the  soft  palate  and  Eustachian  tuhe  is  not  well  known 
as  a  natural  disease,  but  noises  in  the  ears  can  be  induced  in  healthy 
persons  by  the  application  of  the  faradic  or  galvanic  current  to  the  end 
of  the  Eustachian  tube,  which  are  caused  most  probably  by  contraction 
of  the  tubal  muscle.  Twitching  movements  of  the  palate  have  occa- 
sionally been  observed  in  advanced  cases  of  paralysis  agitans. 

(h)  Spasm  of  the  constrictors  of  the  pharynx  usually  accompanies 
acute  pharyngitis  and  spasmodic  stricture  of  the  oesophagus,  while  it  is 
a  prominent  symptom  of  hydrophobia. 

(c)  (Esophagismus,  or  spasmodic  stricture  of  the  oesophagus,  is  fre- 
quently met  Avith  in  hysterical  women,  and  some  believe  that  globus 
hystericus  is  the  subjective  correlative  spasm  of  the  oesophagus.  It 
may  be  so  severe  and  persistent  in  some  cases  of  hysteria  as  to  simulate 
organic  stricture,  and  the  patient  may  be  reduced  to  the  verge  of  death 
by  inanition.  It  is  sometimes  caused  by  irritation  in  the  peripheral 
course  of  the  nerves,  or  in  a  reflex  manner  in  cases  of  ulcer  of  the  tube, 
but  it  is  rare  as  a  result  of  central  disease. 

(2)  Spasmodic  Affections  of  the  Larynx. 

(a)  SPASM  or  the  glottis  in  infants  or  internal  convulsions 
(laryngismus  stridulus). 

Etiology. — The  predisposing  causes  of  spasm  of  the  glottis  in  inftmts 
are  the  same  as  those  which  tend  to  produce  eclampsia,  and,  indeed, 
the  two  diseases  frequently  coexist.  Spasm  of  the  glottis  usually 
attacks  children  between  four  and  ten  months  of  age :  it  is  more  fre- 


300  SPASMODIC    DISORDEES. 

([uent  in  boys  than  in  girls ;  and  badly  nourished,  cachectic,  or  rachitic 
children  are  almost  exclusively  affected.  The  exciting  causes  are  expo- 
sure to  cold,  the  irritation  of  teething,  or  the  presence  of  parasites  or 
other  irritating  substances  in  the  alimentary  canal.  It  may  sometimes 
be  caused  by  direct  irritation  of  the  laryngeal  mucous  membrane  from 
excessive  crying. 

Sympt07m. — The  attack  generally  begins  suddenly  without  premoni- 
tory symptoms,  and  inasmuch  as  the  action  of  the  adductors  predominates 
over  that  of  their  antagonists  the  glottis  is  completely  closed  during 
the  continuance  of  the  spasm.  The  attack  is  characterized  by  a  sudden 
arrest  of  respiration ;  the  chest  becomes  fixed :  the  face  is  turgid  and 
of  a  blue  color;  the  countenance  expresses  great  anxiety:  the  mouth  is 
widely  open,  as  if  to  make  a  deep  inspiration  ;  the  head  is  drawn  back- 
wards ;  the  eves  are  staring ;  the  action  of  the  heart  is  tumultuous  and 
irregular;  and  the  infant  appears  to  be  on  the  verge  of  suffocation, 
then  the  spasm  relaxes.  The  paroxysm  lasts  from  two  to  twenty  sec- 
onds, and  the  end  is  announced  by  a  series  of  sonorous  inspirations,  as 
if  air  were  drawn  through  a  narrow  reed.  The  last  inspiration  becomes 
longer  and  more  sonorous  than  the  rest,  and  then  the  respirations 
assume  their  natural  rhythm.  During  the  paroxysm  the  spasm  involves 
the  extremities,  causing  flexion  of  the  hand  and  extension  of  the  feet, 
and  occasionally  the  infant  is  seized  with  general  epileptiform  convul- 
sions at  the  end  of  the  attack.  The  disease  may  be  limited  to  a  single 
paroxysm,  but  it  usually  consists  of  a  series  of  paroxysms,  coming  on  at 
irregular  intervals  for  many  days  or  weeks.  The  mortality  of  the  dis- 
ease is  very  great,  death  occurring  suddenly  .by  suffocation  during  an 
attack,  or  from  nervous  exhaustion  from  frequently  repeated  attacks. 


(6)    SPASM  OF  THE  GLOTTIS  IN  ADULTS. 

Spasm  of  the  glottis  in  adults  may  be  caused  by  local  disease  of  the 
larynx,  the  inhalation  of  irritating  gases,  tlie  entrance  of  morsels  of 
food  into  the  larynx,  or  irritation  of  one  of  the  recurrent  laryngeal  or 
pneumogastric  nerves.  It  may  also  be  caused  by  centi-al  diseases  of  the 
nervous  system,  like  hysteria.  Paroxysms  of  hysteria  generally  culmi- 
nate in  a  deep  stridulous  inspiration  and  opisthotonos.  On  laryngo- 
scopic  examination  during  an  attack  of  spasm  the  mucous  membrane 
may  be  found  to  be  healthy  or  slightly  congested,  and  the  vocal  cords 
may  be  seen  separating  for  an  instant,  and  then  becoming  spasmodically 
closed. 


SPINO-XEUEAL    SPASMS.  gOl 

(c)    SPASM  OF  THE  TENSOKS  OF  THE  VOCAL  CORDS   (APHONIA  SPASTICA). 

This  condition  does  not  interfere  with  the  respiratory  function,  but 
the  voice  is  rendered  feeble,  jerky,  and  intermittent.  The  patient  may 
speak  a  few  words  in  a  normal  voice,  but  the  current  of  the  voice  is 
soon  partially  interrupted,  and  the  sound  becomes  like  the  suppressed 
voice  of  a  jjcrson  engaged  in  some  act  requiring  a  straining  effort,  like 
the  act  ()f  defecation. 

(d)    SPASMODIC  LARYNGEAL  COUGH. 

The  cough  caused  by  spasm  of  the  laryngeal  muscles  is  a  shrill  or 
barking  cough  of  metallic  quality,  which  comes  on  in  paroxysms  and 
lasts  for  many  hours,  only  ceasing  when  the  patient  sleeps.  This 
cough  occurs  in  young  girls,  but  is  occasionally  met  with  in  hojs.  The 
paroxysmal  cough  of  whooping-cough  is  caused  by  a  direct  or  reflex  irri- 
tation of  the  laryngeal  nerves.  The  attack  begins  with  a  deep  inspira- 
tion, which  is  followed  by  a  succession  of  short  and  frequently  repeated 
coughs  with  no  intervening  inspirations.  When  the  chest  is  contracted 
to  the  utmost,  and  the  patient  seems  on  the  verge  of  asphyxia,  another 
deep  inspiration  is  taken,  during  Avhich  the  air,  rushing  through  the 
spasmodically  closed  glottis,  makes  a  characteristic  whistling,  crowins, 
or  whooping  noise. 

(e)    TABETIC  LARYNGEAL  CRISES. 

The  course  of  locomotor  ataxia  is  liable  to  be  complicated  by  parox- 
ysms of  spasmodic  cough,  not  unlike  those  of  whooping-cough,  and  which 
have  been  named  laryngeal  crises.  These  attacks  may  be  divided  into 
three  varieties  according  to  their  degree  of  intensity :  (a)  the  mild ;  (h) 
the  medium  ;  and  (c)  the  severe  crises. 

(a)  The  mild  attacks  are  like  paroxysms  of  whooping-cough,  the  dura- 
tion of  each  varying  from  a  few  seconds  to  about  ninety. 

[h)  The  medium  form  is  characterized  by  a  more  violent  cough  and 
a  louder  and  more  difficult  inspiration,  the  duration  of  the  attack  being 
from  five  to  ten  minutes. 

(c)  The  severe  form  is  manifested  by  symptoms  of  asphyxia,  uncon- 
sciousness, and  epileptiform  convulsions,  and  the  attack  may  last  from 
half  an  hour  to  several  hours. 

The  attacks  vary  greatly  in  their  periods  of  recurrence ;  they  are 
more  frequent  during  the  day  than  during  the  night,  and  they  may 
sometimes  be  repeated  as  often  as  fifty  times  in  the  twenty-four  hours. 
The  attack  mav  be  excited  by  a  current  of  air,  sudden  exertion,  or  a 


302  SPASMODIC    DISOEDERS. 

slight  catarrli,  or  it  may  come  on  suddenly,  and  without  warning,  in 
the  middle  of  a  conversation  or  during  sleep.  At  other  times  the 
patient  may  feel  a  scalding  sensation,  or  a  feeling  as  if  a  foreign  body 
were  lodged  in  the  larynx,  immediately  before  the  attack. 

(  f)    CLONIC  SPASM  OF  THE  LARYNGEAL  MUSCLES  (CHOREA  OF  THE  LARYNX). 

In  some  cases  the  laryngeal  muscles  contract  and  relax,  during  attempts 
at  phonation  in  such  a  way  that  the  glottis  is  alternately  closed  and 
opened  in  an  irregular  manner,  so  that  the  power  of  inflecting  the  voice 
is  diminished.  Gerhardt  reports  the  case  of  a  flutist  who  was  not  able 
to  play  his  instrument  without  a  continuous  noise  being  caused  in  his 
throat,  and  he  believes  that  the  aff'ection  is  analogous  to  professional 
spasms  in  the  hand.  The  laryngeal  muscles  are  subject  to  clonic 
spasms  in  chorea,  and  in  bilateral  athetosis,  while  they  are  occasionally 
aifected  by  incoordinate  movements  in  ataxia. 

/.    Spasm  in  the  Region  of  the  External  Branch  of  the  Spinal 
Accessory  Nerve  ( Wry-nech,  Caput  Ohstipum  Spasticum). 

Etiology. — The  relatives  of  those  suffering  from  wry-neck  are  often 
subject  to  hysteria  and  other  nervous  affections ;  the  male  sex  is  rather 
more  frequently  affected  than  the  female,  and  adults  than  young  or  old 
people.  The  most  usual  exciting  causes  are  excessive  exertion,  emo- 
tional excitement,  exposure  to  cold,  irritation  of  remote  organs,  while 
it  sometimes  comes  on  suddenly  Avithout  assignable  cause. 

Symptoms. — Spasms  of  the  muscles  supplied  by  this  nerve  may  be 
divided  into,  a,  tonic  and,  6,  clonic  wry-neck. 

(a)  The  tonic  form  is  almost  exclusively  confined  to  one  of  the  sterno- 
cleido-mastoid  muscles,  but  a  part  of  the  trapezius  is  sometimes  aff'ected. 
In  this  form  of  the  disease  the  head  is  rotated  so  that  the  occiput  is 
approximated  to  the  shoulder  of  the  aff'ected  side ;  the  ear  of  the  same 
side  is  drawn  towards  the  clavicle ;  and  the  chin  is  turned  upwards  and 
towards  the  opposite  side.  In  chronic  cases  a  spinal  curvature  with  its 
convexity  to  the  sound  side  occurs  in  the  cervical  region,  and  compensa- 
tory curves  in  the  dorsal  and  lumbar  regions. 

When  the  trapezius  alone  is  the  seat  of  the  spasm  the  head  is  drawn 
strongly  backwards  and  is  inclined  to  the  opposite  side ;  there  is  no  turn- 
ing of  the  chin ;  the  point  of  the  shoulder  is  elevated ;  and  on  any 
attempt  being  made  to  bend  the  head  forwards  the  muscle  becomes  tense 
and  painful  (Fig.  89). 

{h)  The  clonic  form  of  the  disease  may  be  either  unilateral  or 
bilateral. 


S  P  I  K  O  -  X  E  U  R  A  L    SPASMS, 


803 


The  unilateral  variety  begins  with  uneasiness  in  the  neck,  and  it  is 
soon  noticed  by  the  patient  or  his  friends  that  the  head  is  not  stniio-ht. 
As  the  disease  advances  the  patient  comphiins  of  a  dull  achino-  pain  in 
the  course  or  at  the  insertion  of  the  muscle,  and  when  the  spasm  is 
limited  to  one  of  the  sterno-cleido-mastoid  muscles,  the  head  becomes 
rotated  obliquely  to  one  side  by  a  succession  of  jerks,  the  occiput  beino- 
turned  towards  the  shoulder  and  depressed,  and  the  chin  elevated  in  the 
opposite  direction.  The  muscles  on  the  side  to  -which  the  head  is 
drawn  are  hard,  contracted,  and  frequently  hypertrophied.  When  the 
trapezius  is  affected,  the  head  is  bent  back  and  the  shoulder  raised  in 
the  manner  already  described.     At  the  end  of  a  short  time,  generallv  a 

Fig.  89. 


Spasm  of  the  Tkapezius.     (Fioni  Dlchexxe  ) 


few  seconds,  the  muscle  relaxes  and  the  head  returns  to  the  normal 
position,  but  this  is  soon  followed  by  a  second  contraction  and  a  second 
rotation.  At  first  there  may  be  a  considerable  interval  between  the 
contractions,  but  as  the  disease  advances  the  interval  is  shortened,  and 
ultimately  the  contractions  may  number  twenty  or  thirty  in  the  minute. 
In  an  early  stage  the  patient  may  arrest  the  spasm  by  a  voluntary 
effort,  or  counteract  it  by  a  voluntary  contraction  of  the  muscles  of  the 
opposite  side,  but  in  long-standing  cases  the  voluntary  is  overpowered 
by  the  involuntary  contractions,  and  the  head  is  habitually  twisted  to 
one  side,  except,  indeed,  when  the  patient  counteracts  the  deformity  by 
holding  his  head  between  both  hands,  or  placing  it  against  a  resisting 


;304  SPASMODIC    DISORDERS. 

object.  Patients  are  distressed  by  wakefulness  caused  by  constant  move- 
ments of  the  head  against  the  pillow,  but  as  sleep  is  approaching  they 
feel  the  movements  becoming  gradually  less,  and  the  spasm  generally 
ceases  entirely  during  sleep. 

The  disease  is  rarely  confined  to  the  muscles  supplied  by  the  spinal 
accessory  nerve,  and  it  is  even  probable  that  the  splenii  and  obliqui 
capitis  are  often  the  first  attacked,  and  they  are  at  least  generally  impli- 
cated. When  the  scaleni  are  affected  oedema  and  some  degree  of  anes- 
thesia of  the  corresponding  arm  may  be  present  from  compression  of 
the  brachial  plexus  and  veins.  Facial  tic  and  masticatory  spasm  may 
be  associated  with  clonic  spasmodic  torticollis,  and  in  aggravated  cases 
the  spasm  extends  to  the  muscles  supplied  by  the  cervical  and  brachial 
plexuses.  The  clonic  form  of  the  disease  is  generally  unilateral,  but 
occasionally  the  spasm  invades  both  sides,  and  then  the  head  is  rotated 
first  to  the  one  side,  and  after  a  time  to  the  other,  according  as  the 
action  of  the  muscles  of  one  side  or  of  the  other  predominates.  Occa- 
sionallv  the  two  muscles  may  hai)pen  to  contract  simultaneously,  and 
the  head  is  then  bent  forwards  and  the  chin  drawn  to  the  sternum. 
The  faradic  irritability  of  the  affected  muscles,  and  the  faradic  sensi- 
bility of  that  side  are  increased.  A  constant  current  of  moderate 
strength  may  relax  the  spasm  for  a  moment,  but  it  soon  returns  when 
the  current  is  Avithdrawn.  Points  of  arrest  are  frequently  found  in  the 
course  of  the  nerve  or  over  the  affected  muscles. 

The  bilateral  clonic  Avry-neck  (eclampsia  nutans,  salaam  convulsion) 
is  almost  exclusively  met  with  in  children  from  the  first  period  of  den- 
tition to  puberty.  The  spasm  comes  on  in  paroxysms,  each  of  which 
lasts  only  from  a  few  seconds  to  some  minutes,  but  generally  recurs 
two  or  three  times,  or  many  times  in  the  course  of  the  day.  During 
the  attack  the  body  and  head  are  bent  slightly  forwards,  and  this  is 
followed  by  almost  instantaneous  relaxation,  to  be  succeeded  after  an 
interval  of  a  few  seconds,  by  a  second  bowing  of  the  head,  and  so  on 
until  the  paroxysm  ceases  after  from  twenty  to  one  hundred  alternate 
contractions  and  relaxations.  The  spasm  in  the  neck  has  frequently 
associated  with  it  some  degree  of  facial  spasm,  Idepharospasm,  strabis- 
mus, or  a  slight  convulsive  movement  of  one  or  other  arm,  and  at  other 
times  attacks  of  general  convulsions  intervene,  so  that  the  case  becomes 
manifestly  one  of  ordinary  epilepsy.  During  the  attack  the  child 
seems  bewildered,  but  there  is  no  complete  loss  of  consciousness,  and 
as  soon  as  the  movements  cease  the  patient  may  be  ([uite  bright  and 
happy,  but  occasionally  the  attack  is  followed  by  exhaustion  and 
<lrowsiness. 


SPIXO-NEURAL    SPASMS. 


305 


(J.  Sjyasm  of  the  Musdes  supplied  by  the  Cervical  Plexus. 

(1)  Spasm  of  the  Muscles  of  the  Neck. 

(a)  Spasm  of  the  splenius  capitis  causes  the  head  to  be  drawn  back- 
wards and  towards  the  affected  side  (Fig.  90),  and  the  chin  to  be  some- 

FiG.  no. 


Spasm  of  Splenus 


what  depressed  and  directed  towards  the  aftected  side,  Avhile  a  hard 
ridge  can  be  felt  at  the  point  where  the  splenius  appears  beneath  the 
anterior  l)order  of  the  trapezius.  The  spasm  is  generally  tonic  with 
remissions  and  occasional  more  energetic  contractions. 

(h)  Spasm  of  the  ohliquus  capitis  inferior  causes  either  intermittent 
or  persistent  rotation  of  the  head  around  its  vertical  axis  without  eleva- 
tion of  the  chin  or  depression  of  the  mastoid  pi'ocess. 

(e)  Spasm  of  the  deep  muscles  of  the  neck  is  characterized  by 
stronor  backward  rotation  of  the  head  when  the  affection  is  bilateral,  or 
towards  the  affected  side  Avhen  it  is  unilateral. 

(2)  Spasm  of  the  Diaphragm. 

{a)  Tonic  spasm  of  the  diaphragm  causes  so  much  dypsnoea  that  the 
patient  is  threatened  with  asphyxia.  The  lower  half  of  the  chest  is 
expanded  and  immovable,  and  the  epigastrium  is  made  to  project 
strongly,  whilst  rapid  and  superficial  respirations  are  effected  with  the 

20 


806 


SPASMODIC    DISORDERS, 


upper  part  of  the  chest.  There  is  severe  pain  in  the  epigastrium  and 
alon(^  the  attachments  of  the  diaphragm,  the  voice  becomes  feeble  and 
muffled,  there  is  Avell-marked  cyanosis,  and  the  attack  proves  fetal  if  it 
last  beyond  a  short  time. 

{b)  Qlonic  spasm  of  the  diaphragm,  singultus  or  hiccough  consists  of 
short  energetic  contractions  of  the  diaphragm  accompanied  by  an  inspira- 
tory sound,  which  is  usually  suddenly  arrested  by  closure  of  the  glottis. 
The  contractions  may  succeed  each  other  at  tolerably  long  intervals  or 
may  occur  in  rapid  succession,  and  the  attack  may  last  from  a  few 
minutes  to  many  hours,  or,  in  aggravated  cases,  for  weeks,  and  they 
may  recur  more  or  less  fre([uently  for  years.  Hiccough  is  caused  by 
reflex  irritation  from  neighboring  or  remote  organs,  and  it  is  to  be 
regarded  as  an  ominous  sign  in  cancer  of  the  abdominal  viscera  and 
in  cachectic  conditions.  It  is  often  of  hysterical  origin,  and  it  may  be 
caused  by  direct  irritation  of  the  roots  of  the  phrenic  nerves  from  cer- 
vical pachymeningitis. 

h.  Spasm  of  the  3Iusc/cs  supplied  by  the  Brachial  Plexus. 

(1)  Spasm  of  the  Muscles  of  the  Neck  and  Trunk. 
(a)  Spasm  of  the  rhomboidci  manifests  itself  by  the  peculiar  position 
of  the  scapula  (Fig.  91).     Its  inner  border  assumes  an  oblique  position 


ViG.  91. 


Contraction  of  Rhomboid  Muscle.s.    (Duchenne.) 

A,  Levator  scapulae  ;  B,  Ketracted  rhomboid  ;  C,  Fibres  of  serratus  magnus  ;  D,  Abnormal  position  of 

the  inferior  angle  of  the  scapula ;  E,  Inferior  angle  on  the  healthy  side. 


SPINO-NEUEAL    8PASMS.  ;-507 

from  above  dowiuvanls  and  from  within  outwards,  the  lower  an-de  is 
drawn  upwards  and  approximated  to  the  vertebral  column,  the  m'uscle 
can  be  felt  as  a  firm  swelling  between  the  scapula  and  spinal  column, 
and  it  offers  a  distinct  resistance  when  an  attempt  is  made  to  raise  the 
arm  to  a  vertical  position. 

{b)  Spasm  of  the  Levator  Anguli  Seapuke. — The  upper  and  inner 
angle  of  the  scapula  is  strongly  elevated,  the  head  is  slightly  inclined 
to  the  same  side,  the  shoulder  is  drawn  somewhat  forwards,  the  supra- 
clavicular fossa  is  increased  in  depth,  and  the  contracted  muscle  projects 
distinctly  beneath  the  anterior  liorder  of  the  trapezius,  which  can  easily 
be  isolated  from  it  by  faradization. 

(c)  Spasm  of  the  serratus  magnus,  latissimus  dorsi,  the  teres  major 
and  minor,  the  supra-  and  infraspinati,  the  subsrapularis,  or  the  pee- 
toralis  major,  is  rare.  It  may  be  readily  recognized  by  the  position 
assumed  by  the  scapula  and  arm,  and  the  kind  of  interference  with 
their  movement,  along  with  the  hardness  and  fulness  felt  over  the 
affected  muscle.  The  diagnosis  is  aided  by  a  comparison  with  the 
deformity  produced  by  faradization  of  the  corresponding  muscles  of  the 
opposite  side. 

(2)  Spasm  of  the  Muscles  of  the  Upper  Extremity. 

(a)  Spasm  of  the  Muscles  Supplied  by  the  Circumflex  Nerve. — In 
the  tonic  form  of  spasm  the  arm  is  held  out  from  the  body,  and  it  is 
also  directed  backwards  in  those  cases  in  which  the  j)Osterior  fibres  of 
the  deltoid  and  teres  minor  are  aff"ected.  The  lower  angle  of  the  scapula 
is  pressed  backwards  towards  the  vertebral  column,  as  in  paralysis  of 
the  serratus  magnus.  In  cases  of  clonic  spasm  of  the  deltoid  the  arm 
is  thrown  upwards  and  moved  convulsively  in  various  directions,  but 
other  muscles  are  usually  implicated  at  the  same  time. 

(b)  Sjjasm  of  the  muscles  supplied  by  the  musculo-cutaneous  nerve 
causes  some  resistance  to  passive  abduction  of  the  arm,  and  strong 
flexion  of  the  forearm. 

(c)  Spasm  of  the  muscles  supplied  by  the  musculo-spiral  nerve  causes 
extension  of  the  forearm  at  the  elbow,  of  the  hand  at  the  wrist,  of  the 
fingers  at  the  metacarpo-phalangeal  articulations,  and  of  the  thumb  at 
both  the  metacarpo-phalangeal  and  phalangeal  articulations,  as  well  as 
supination  of  the  forearm. 

(d)  Spasm  of  the  Muscles  Supplied  by  the  Median  Nerve. — In  spasm 
of  these  muscles  the  forearm  is  strongly  pronated ;  the  hand  is  bent 
towards  the  radial  side  ;  the  fingers  are  flexed ;  and  there  is  apposition 
of  the  thumb.     Spasm  of  the  muscles  of  the  hand  supplied   l)y  the 


308  SPASMODIC    DISOEDEKS. 

median  produces  apposition  of  tlie  thumb,  Avith  approximation  and  slight 
flexion  of  the  first  phalanges  of  the  index  and  middle  fingers. 

(e)  Spasm  of  the  3Iusdes  Supplied  by  the  Ulnar  Nerve.— In  spasm 
of  these  muscles  the  hand  is  rendered  concave ;  the  thumb  is  adducted  ; 
the  little  finger  is  strongly  flexed  and  opposed  ;  and  the  remaining 
fingers  are  moderately  flexed  at  the  metacarpo-phalangeal  and  extended 
at  the  phalangeal  articulations.  The  position  assumed  by  the  hand  in 
spasm  of  the  interossei  is  shown  in  Fig.  92. 

Fig.  92. 


Position  of  the  Hand  in  Spasm  of  the  Interosseous  Muscles.    (After  riowEas.) 

(/')  Writer  s  Cramp  and  Allied  Affections  {Graphospasmus,  Mogi- 
l/raphia.  Professional  Hyperkiyieses). — Writer's  cram])  is  only  one  of 
a  large  group  of  aftections  which  have  been  called  professional  hyper- 
kineses.  This  name  has  been  given  to  them  because  the  spasm  aff"ects 
muscles  engaged  in  delicate  associated  and  acquired  actions,  such  as 
those  required  for  writing,  piano-forte  playing,  sewing,  etc. 

Etiology. — Writer's  cramp  is  most  frecjuently  met  with  in  men,  while 
piano-forte  player's  spasm  occurs  most  frequently  in  women.  Profes- 
sional spasms  of  all  kinds  are  liable  to  occur  in  nervous  subjects  and 
neuropathic  families.  The  spasm  may  be  caused  by  exposure  to  cold, 
injuries  of  nerves  or  muscles,  and  foreign  bodies  in  the  fingers,  or  it  may 
be  caused  in  a  reflex  manner  by  periostitis  of  the  external  condyle  of 
the  humerus.  The  main  cause,  however,  of  writer's  cramp  is  excessive 
writing,  and  consequently  it  is  most  frequently  observed  in  secretaries, 
clerks,  and  merchants.  The  other  professional  cramps  are  also  caused 
in  the  same  way  by  the  excessive  use  of  particular  groups  of  muscles. 

Symptoms. — Writer's  cramp  may  be  divided  into  (1)  the  spastic, 
(2)  the  tremulous,  and  (3)  the  paralytic  forms. 

(1)  In  the  spastic  form  of  the  disease  some  of  the  muscles  of  the 
hand  are  seized  with  tonic  or  clonic  spasms  whenever  the  patient  tries 
to  use  the  pen  and  this  gives  rise  to  an  irregular  stroke  in  the  writing. 
The  patient  may,  indeed,  be  quite  unable  to  write  Avhile  holding  his 
pen  in  the  usual  position,  but  he  is  often  able  to  do  so  tolerably  well  by 
holding  it  in  a  new  and  more  or  less  grotesque  manner.     After  a  time 


SPINO-NEUEAL    SPASMS.  309 

the  spasm  becomes  stronger ;  the  thumb  and  first  finger  may  be  sud- 
denly extended  so  that  the  pen  drops,  or  there  is  a  spasmodic  action  of 
the  opponens  pollicis,  with  abduction  and  flexion  of  the  index-finc^er 
and  the  pen  is  thus  rapidly  moved  away  from  the  paper.  At  other 
times  there  is  spasmodic  flexion  of  the  first  three  fingers,  which  then 
become  pressed  tightly  against  the  pen,  so  that  it  cannot  be  moved  fur- 
ther onwards ;  or  there  may  be  movements  of  pronation  and  supination 
in  the  forearm,  and  the  pen  is  raised  from  the  paper,  and  moved  back- 
wards and  forwards  in  the  most  irregular  manner.  The  faradic  con- 
tractility of  the  affected  muscles  is  sometimes  increased,  and  at  other 
times  diminished,  the  former  probably  indicating  an  early,  and  the 
latter  a  late  stage  of  the  affection. 

(2)  In  the  tremulous  form  of  the  disease  the  hand  and  forearm,  or 
even  the  whole  arm,  are  the  subjects  of  Avell-marked  tremors  on  any 
attempt  at  writing,  so  that  the  pen  only  makes  undulating  or  angular 
strokes.  The  writing  is  altered  in  character ;  the  strokes  are  coarse, 
imperfect,  and  unequal,  and  numerous  irregularities  and  false  strokes 
are  to  be  observed,  while  in  the  highest  degrees  of  the  aftection  the 
writing  becomes  a  mass  of  undulating  and  zigzag  strokes,  and  wholly 
illegible. 

(3)  In  the  paralytic  form  the  patient  experiences  great  fatigue  and 
weakness  of  the  hand  and  forearm  on  attempting  to  write,  but  as  soon 
as  the  pen  is  laid  down  the  feeling  of  weakness  and  exhaustion  disap- 
pears, to  reappear  when  it  is  taken  up  again. 

In  those  who  suffer  from  writer's  cramp  the  movements  requisite  for 
sewing,  piano-forte  playing,  embroidery,  buttoning-up  the  clothes,  and 
all  actions  requiring  delicate  manipulation  are  also  impaired ;  and  if 
the  patient  has  learned  to  write  with  his  left  hand,  the  spasm,  to  his 
great  disappointment,  frequently  extends  to  it  also. 

The  most  common  sensory  disorder  is  an  undefined  feeling  of  strain- 
ing and  fatigue,  a  sensation  of  pressure  in  the  affected  muscles,  a  pain- 
ful drawing  of  the  nerves  in  the  direction  of  the  trunk,  or  a  feeling  of 
coldness  in  the  whole  arm. 

The  pain  frequently  extends  to  the  shoulder  and  back,  and  some  of 
the  spinous  processes  of  the  cervical  and  dorsal  vertebrpe  may  be  tender 
to  pressure. 

Other  spasmodic  disorders  are  not  infrequently  associated  with 
writer's  cramp,  the  most  frequent  of  these  being  strabismus,  stammer- 
ing, and  spasms  of  the  face,  throat,  and  other  parts  of  the  body,  while 
weakness  and  tremors  of  the  lower  extremities  occasionally  occur.  In 
addition  to  the  mental  depression  caused  by  failure  of  the  hand  the 
patient  is  often  of  an  anxious  disposition,  and  subject  to  general  nei-v- 


310  SPASMODIC    DISORDERS. 

ousness,  which  makes  tlie  writing  worse  when  executed  in  the  presence 
of  a  spectator. 

The  following  are  a  few  of  the  other  professional  hjperkineses : 

Piano-forte  player  s  spasm  is  not  uncommon  in  professional  players, 
especially  women,  and  the  spasm  is  in  every  respect  similar  to  that  of 
writer's  cramp. 

Telegraphist's  cramp  has  been  met  in  France  with  the  use  of  Morse's 
machine,  in  which  the  letters  are  represented  by  an  association  of  dashes 
and  dots. 

Violin-player's  spasm  occurs  either  in  the  form  of  painful  exhaus- 
tion and  stiffness,  or  as  a  convulsive  spasm  of  some  of  the  muscles  of 
the  hand,  arm,  or  shoulder.  It  may  attack  the  right  or  left  hand,  and 
it  renders  playing  impossible. 

Tailor  s  and  shoemaker  s  spasw  is  of  the  same  kind  as  the  other 
professional  spasms,  and  as  soon  as  the  patient  begins  to  Avork,  tonic  or 
clonic  spasms,  or  functional  debility  of  the  muscles  of  the  hand  and 
arm,  are  experienced. 

Spasmodic  movements  have  been  described  as  occurring  in  smiths, 
milkers,  painters,  makers  of  artificial  flowers,  harp-players,  turners, 
and  watchmakers. 

i.    Spasms  of  the  Muscles  supplied  hy  the  Dorsal  Nerves. 

(1)  Spasms  of  the  Kespikatory  Muscles. 

{a)  Inspiratory  spasni  differs  considerably  from  hiccough,  although 
the  latter  frequently  complicates  the  former.  The  essential  feature  of 
the  affection  is  that  many  or  all  of  the  muscles  particii)ate  in  the 
spasm,  and  that  a  true  inspiration,  unbroken  by  sudden  closure  of  the 
glottis,  takes  place.  The  spasm  consists  of  a  more  or  less  rapid  suc- 
cession of  deep  inspirations,  whilst  the  intervening  expirations  are  per- 
formed in  the  usual  noiseless  way.  The  chest  is  powerfully  expanded, 
the  epigastrium  is  protruded,  the  auxiliary  muscles  of  respiration  are 
excited  to  action,  the  pectoral  and  sterno-cleido-mastoid  muscles  are 
brought  into  strong  relief,  the  shoulders  are  raised,  the  head  is  drawn 
backwards,  and  the  respiratory  muscles  of  the  face,  ala  nasi,  and  eye- 
lids enter  into  strong  contraction.  Inspiration  is  noisy,  and  often 
accompanied  by  eructations  of  gas  from  compression  of  the  stomach. 
The  spasm  usually  occurs  in  paroxysms  of  variable  duration,  the  ab- 
domen is  generally  tympanitic,  and  there  are,  as  a  rule,  other  symptoms 
of  nervous  derangement,  especially  those  characteristic  of  hysteria. 

{b)  Attacks  of  sneezing  {sternutatio  eonvulsiva)  occur  in  a  parox- 
ysmal and  spasmodic  form,  so  that  the  patient  will  sometimes  sneeze 


SPTNO-NEURAL    SPASMS.  311 

several  hundred  times  in  succession.  Ordinary  sneezino-  is  a  reflex 
act  excited  by  irritation  of  the  nasal  filaments  of  the  fifth  nerves. 
Attacks  of  sneezing  are  generally  accompanied  by  a  profuse  watery 
secretion  from  the  nose,  and,  when  of  long  duration,  they  are  produc- 
tive of  great  misery. 

{(■)  Attacks  of  y<iwning  {osredo,  chasme)  consist  of  a  succession  of 
yawns  following  one  another  with  greater  or  less  rapidity,  and  are 
accompanied  l)y  the  well-known  phenomenon  of  gaping,  flow  of  saliva, 
increased  flow  of  tears,  and  diminution  in  the  acuteness  of  hearing, 
with  dull  tinnitus  aurium. 

(d)  Spasmodic  cough  comprises  all  those  paroxysmal  attacks  of 
coughing  Avhich  are  accompanied  by  a  loud  ringing  sound.  Such 
attacks  of  coughing  may  last  for  a  variable  ])eriod,  and  may  also  recur 
frequently  for  months  or  years. 

{e)  Fits  of  laughin;)  or  crying  are  a  form  of  expiratory  spasm,  the 
former  consisting  of  a  succession  of  loud  expirations  accompanied  by 
vocal  tones,  and  the  latter  of  long-drawn  expirations,  often  interrupted 
by  sobs  and  generally  by  a  profuse  secretion  of  tears.  These  actions 
are  accomjianied  by  well-known  mental  states,  and  by  characteristic 
fecial  expressions.  In  pathological  conditions  they  may  be  independent 
of  emotional  disturbances,  and  they  then  constitute  subordinate  symp- 
toms of  several  general  neuroses,  such  as  hysteria,  or  are  produced  by 
disease  of  the  central  nervous  system. 

(/)  Spasm  of  the  Dorsal  and  Abdominal  Muscles. — The  dorsal 
muscles  are  the  subjects  of  a  strong  tonic  spasm  in  tetanus,  and  some- 
times in  hysteria,  wdiile  they  are  affected  by  both  tonic  and  clonic 
spasm  in  attacks  of  epilepsy  and  eclampsia.  They  may  also  be  affected 
by  spasm  in  cases  of  lateral  spinal  sclerosis,  and  various  other  central 
aff'ections.  The  abdominal  muscles  are  also  ;iffected  by  spasm  in  cen- 
tral nervous  affections,  and  they  are  the  subjects  of  spasm  in  l)iliary 
calculi  and  all  ])ainful  affections  of  the  abdominal  organs.  In  spasm 
of  the  muscles  of  the  l»ack  the  body  is  strongly  arched  backwards,  a 
condition  which  has  been  named  opisthotonos,  or  when  the  action  of 
the  muscles  of  one  side  predominates  it  is  arched  backwards  and  to 
one  side,  a  condition  named  pleurosthotonos. 

In  spasm  of  the  abdominal  muscles  the  walls  of  the  abdomen  become 
hard,  tense,  and  resisting,-  and  as  it  is  generally  accompanied  by  spasm 
of  the  dia})hragm,  the  breathing  is  of  the  upper  costal  type,  and  be- 
comes accelerated  and  shallow. 


312  SPASMODIC    DISORDERS. 

h.  Spasm  of  the  Muscles  supplied  hy  the  Lumbar  and  Sacral  Nerves. 

(1)  Spastic  contracture  of  the  hip  consists  of  a  tonic  spasm  of  the 
psoas  and  iliacus,  the  quadratus  lumborura,  and  occasionally  of  one  or 
two  of  the  muscles  of  the  front  of  the  thigh.  The  extremity  is  flexed 
at  the  hip-joint,  the  tendon  and  muscular  belly  of  the  ilio-psoas  muscle 
project  strongly,  the  pelvis  appears  to  be  raised  on  the  aftected  side, 
the  limb  is  shortened,  and  the  patient  inclines  to  the  afiected  side  in 
walking.  Any  attempt  to  extend  the  limb  causes  acute  pain  in  the 
tense  muscles  and  in  the  knee.  This  aifection  is  caused  by  disease  of 
the  lumbar  vertebrae  with  psoas  abscess,  and  by  reflex  irritation  in 
disease  of  the  hip-joint. 

(2)  Spasm  of  the  quadriceps  extensor  femoris  gives  rise  to  rigid 
extension  of  the  leg  on  the  thigh,  and  is  observed  in  tetany  and  neu- 
ralgia of  the  knee-joint.  Clonic  spasm  of  the  extensors  of  both  sides 
was  observed  in  a  case  in  which  no  obvious  cause  could  be  traced. 
The  spasms  recurred  at  brief  but  irregular  intervals,  and  gave  a  pecu- 
liar hopping  character  to  the  gait. 

(3)  Contracture  of  the  adductors  of  both  thighs  approximates  the 
knees  together,  and  is  a  symptom  of  lateral  sclerosis  of  the  spinal  cord. 
It  also  occurs  in  tetany,  and  is  probably  caused  sometimes  by  reflex 
irritation  from  disease  of  the  hip-joint,  or  from  genital  irritation. 

I.   Spasm  of  the  Muscles  supplied  hy  the  Sciatic  Nerves. 

(1)  Spasm  of  the  flexors  of  the  leg  causes  the  leg  to  be  flexed  on 
the  thigh,  and  in  aggravated  cases  the  heel  is  brought  in  contact  with 
the  buttocks.  It  occurs  in  hysteria,  diseases  of  the  knee-joint,  and 
spinal  diseases. 

(2)  Spasm  of  the  anterior  muscles  of  the  leg  is  of  rare  occurrence. 
A  painful  contracture  of  the  tibialis  anticus,  peroneus  longus,  and  gas- 
trocnemius is  described  by  Dr.  S.  Weir  Mitchell  as  occurring  in  young 
people  after  long  standing,  and  leading  to  deformity  of  the  feet. 
Spasm  of  the  peroneus  -  longus  plays  an  important  part  in  the  produc- 
tion of  certain  forms  of  club-foot,  and  is,  according  to  Duchenne,  of  two 
kinds,  the  first  consisting  of  persistent  contraction  of  the  muscle ;  the 
second  of  a  functional  spasm  which  occurs  only  when  the  leg  is  brought 
into  use.  The  latter  form  is  particularly  liable  to  occur  in  congenital 
spasmodic  aflections. 

(3)  Spasm  of  the  muscles  of  the  calf  produces  talipes  equinus,  in 
which  the  heel  is  strongly  elevated  and  the  toes  depressed.     The  well- 


SPINO-NEURAL    SPASMS.  813 

known  "cramps"  of  the  calf  belong  to  this  variety,  and  it  occurs  in 
sciatica  and  painful  affections  of  the  knee-joint. 

(4)  Diffused  spasm  of  the  muscles  of  the  lower  extremity  of  one  or 
both  sides  occurs  in  hysteria,  as  a  motor  aura  in  epilepsy,  and  in  spinal 

diseases. 

2.  General  Spino-neural  Spasms. 

a.    Saltatory  Spasm. 

Etiology. — In  all  cases  of  this  disease  either  a  decided  neuropathic 
disposition  has  been  clearly  traceable  or  the  patients  themselves  have 
been  subjected  to  depressing  influences  before  the  attack.  The  male  is 
as  frequently  attacked  as  the  female  sex,  and  the  ages  of  those  aftected 
range  from  ten  to  seventy  years. 

Symptoms. — In  this  affection  singular  spasms  of  the  muscles  of  the 
lower  extremities  arise  when  the  sole  of  the  foot  is  placed  upon  the 
ground,  which  have  the  effect  of  throwing  the  patient  repeatedly  in  the 
air.  These  spasms  continue  so  long  as  the  patient  maintains  the  erect 
posture,  and  they  cause  the  patient  to  hop  and  jump  on  the  floor,  and 
render  him  quite  unable  to  stand  still  for  an  instant.  In  some  cases 
the  feet  are  thrown  oft'  the  ground  at  every  spring,  and  in  others  the 
hopping  movements  are  caused  by  quickly  alternating  elevations  and 
depressions  of  the  heel,  while  in  one  of  two  cases  reported  by  Gowers, 
the  springing  movements  w^ere  made  from  the  hip  and  knee-joints. 
The  movements  disappear  when  the  patient  sits  or  lies  down,  but  in 
most  cases  they  can  be  made  to  reappear  by  pressing  on  the  soles  of  the 
feet.  The  onset  of  the  symptom  is,  as  a  rule,  more  or  less  sudden,  but 
in  a  few  cases  premonitory  symptoms  such  as  a  sense  of  w^eight,  tearing 
pains,  or  slight  tremors,  have  been  observed.  The  spasms  may  disappear 
in  a  few  days  or  last  for  many  weeks,  and  they  may  recur  after  a  per- 
fectly free  interval.  The  distribution  of  the  spasms  varies  greatly,  they 
are  at  times  limited  to  the  legs,  while  at  other  times  they  extend  to  the 
muscles  of  the  back,  face,  neck,  and  pupils,  but  the  arms  always  remain 
unaffected.  Emotional  excitement  has  sometimes  been  found  to  aggravate 
the  spasm  and  at  other  times  to  arrest  it. 

h.   Tetanus. 

Etiology. — Tetanus  may  be  of  traumatic  or  idiopathic  origin.  Trau- 
matic tetanus,  which  is  by  for  the  more  important  and  frequent  variety, 
is  caused  by  punctured,  lacerated,  or  contused  wounds,  and  may  even 


;->14  SPASMODIC    DISORDERS. 

result  from  contusions  without  external  abrasion,  but  is  rare  after  incised 
wounds.  The  extent  and  severity  of  the  wound  do  not  appear  to  bear 
any  direct  relation  to  the  frequency  of  tetanus,  and  in  some  cases  the 
primary  wound  is  healed  and  forgotten  when  the  symptoms  make  their 
api>eai-ance.  The  interval  between  the  injury  and  the  development  of 
tetanus  varies ;  the  average  duration  is  from  four  to  fourteen  days,  but 
the  symptoms  may  begin  in  a  few  hours  or  be  delayed  many  weeks  after 
the  injury.  Various  causes  may  cooperate  with  the  external  wound  in 
the  production  of  tetanus,  the  most  potent  of  these  being  exposure  to  cold 
and  damp  after  the  patient  has  undergone  great  excitement  and  fatigue 
like  that  caused  l)y  a  great  battle.  The  absence  of  antiseptic  dressings 
and  other  improper  treatment  seem  to  increase  the  liability  to  tetanus. 

The  most  usual  cause  of  idiopathic  tetanus  is  exposure  to  cold  and 
damp,  more  especially  when  the  patient  is  warm  and  perspiring.  It  may 
occur  in  the  course  of  pleurisy,  peritonitis,  and  other  acute  diseases. 
Malaria  appears  to  give  rise  occasionally  to  an  intermittent  tetanus  which 
may  be  cured  by  quinine.  Strychnine  and  other  toxic  agents  cause 
symptoms  resembling  tetanus. 

Symptoms. — Premonitory  symptoms  are  generally  observed  in  tetanus, 
consisting  of  shivering  or  a  distinct  rigor,  sensation  of  dragging  in  the 
neck,  stiffness  in  certain  muscles,  difficulty  of  articulation  and  degluti- 
tion, and  yawning.  In  traumatic  cases  the  wound  may  become  sensitive, 
and  the  patient  complain  of  shooting  pains  radiating  from  it.  These 
symptoms  may  occur  a  few  hours  or  even  a  few  days  before  the  charac- 
teristic tonic  spasms  make  their  appearance. 

The  spasms,  as  a  rule,  begin  in  the  muscles  of  the  jaw.  At  first  the 
jaws  can  be  separated,  and  the  movements  of  cheAving  and  swallowing 
be  accomplished,  although  with  difficulty.  Soon,  however,  the  jaws 
become  firmly  clenched,  constituting  the  condition  called  trismus ; 
swallowing  of  even  a  small  quantity  of  fluid  is  difficult  and  fatiguing 
owing  to  spasm  of  the  <x\sophagus ;  while  articulation  is  indistinct,  and 
the  voice  altered,  partly  from  the  difficulty  of  moving  the  toncrue,  and 
partly  from  implication  of  the  muscles  of  tlie  larynx. 

Spasm  of  the  facial  muscles  gives  to  the  countenance  a  characteristic 
expression.  The  angles  of  the  mouth  are  drawn  outwards,  being  at  the 
same  time  depressed  or  elevated,  and  the  lips  are  often  drawn  apart  and 
expose  the  set  teeth,  so  that  the  face  assumes  a  sneering  expression, 
named  the  "n-SMS  sardonicus."  The  nostrils  are  dilated ;  the  eyes  are 
staring  and  motionless  ;  the  pupils  are  generally  contracted ;  the  brow 
IS  wrinkled ;  and  all  the  lines  of  the  face  become  strongly  marked,  and 
give  to  the  patient  an  aged  appearance. 

The  spasm  rapidly  extends  to  the  muscles  of  the  back  of  the  neck, 


SPINO-NEUKAL    SPASMS.  315 

causing  retraction  of  the  head ;  while  the  erectove  spinae  soon  become 
implicated,  and  the  vertebral  column  is  then  arched  backwards;  the 
chest  is  projected  forwards  and  rendered  very  broad  ;  and  the  body  rests 
on  the  back  of  the  head  and  sacrum,  constituting  the  condition  called 
opisthotonos.  The  epigastrium  is  sunk,  and  the  abdomen  flattened, 
while  the  hardness  assumed  by  the  abdominal  muscles  is  characteristic. 
On  rare  occasions  the  body  is  said  to  be  bent  forwards,  the  convexity  of 
the  arch  being  directed  backwards,  a  condition  named  emprosthotonos. 
In  a  few  cases  the  bodv  is  maintained  in  a  rigid  attitude  without  beino- 
curved  in  any  direction,  a  condition  named  orthotonos ;  and  in  some 
rare  cases  it  is  curved  laterally — plcurosthotonos. 

The  muscles  of  the  extremities  are  usually  not  affected  to  so  great 
an  extent  as  those  of  the  trunk,  neck,  lace,  and  jaws.  The  muscles  of 
the  lower  extremities  are,  however,  generally  implicated  to  a  greater  or 
less  extent ;  and  extension,  as  a  rule,  predominates  over  flexion  during 
the  spasmodic  attack,  although  flexion  at  individual  joints  has  occasionally 
been  observed.  During  the  attack  the  varioris  segments  of  the  lower 
extremities  are  extended  upon  one  another  and  upon  the  trunk,  so  that 
the  patient  rests  on  the  head  and  heels ;  the  toes  are  extended  and 
spread  out ;  and  the  feet  are  everted.  Even  in  severe  cases  the  muscles 
of  the  upper  extremities  may  remain  comparatively  unaffected,  but  if 
passive  motion  of  the  forearm  be  attempted,  increased  muscular  resistance 
is  readily  perceived.  When  the  spasm  extends  to  the  muscles  of  the 
upper  extremities,  flexion  predominates  over  extension  ;  and  during  the 
paroxysms  the  arms  are  drawn  close  to  the  chest ;  the  forearm  is  flexed 
upon  the  arm  ;  the  hand  is  flexed  at  the  wrist;  and  the  fist  is  closed, 
the  palm  being  directed  towards  the  upper  arm  (Fig.  93). 

In  some  cases  the  spasm  persists  continuously  from  the  beginning  to 
the  termination  of  the  disease ;  but,  as  a  rule,  the  spasmodic  rigidity 
of  the  muscles  occurs  in  paroxysms  with  intervals  of  comparative,  but 
never  complete  muscular  relaxation.  Each  paroxysm  lasts  from  a  few 
seconds  to  several  minutes,  or  with  slight  remissions  for  hours ;  while 
the  duration  of  the  free  interval  varies  from  ten  minutes  to  hours,  but 
at  other  times  the  spasms  recur  and  remit  with  such  frequency  that  they 
assume  a  more  or  less  clonic  character.  As  the  disease  progresses,  the 
paroxysms  of  spasm  recur  with  greater  frequency,  and  muscular  con- 
traction is  sometimes  so  violent  that  teeth  are  broken,  long  bones  frac- 
tured and  powerful  muscles  torn  across.  The  paroxysms  recur  spon- 
taneously, but  they  are  induced  by  the  most  trivial  external  cause,  such 
as  a  draught  of  air,  a  sudden  noise,  or  an  attempt  to  swallow  or  to 
administer  an  injection.  Attempts  at  swallowing  may,  indeed,  provoke 
an  attack  so  readily  that  the  disease  may  bear  a  certain  resemblance  to 


516 


SPASMODIC    DIS0EDEE3. 


hydrophobia.  The  spasm  occasioned  by  the  attempt  may  be  in  the 
pharynx,  gullet,  or  in  the  cardiac  end  of  the  stomach,  as  the  oesophagus 
passes  through  the  diaphragm.  But  wherever  it  may  be  situated,  all 
attempts  at  swallowing  are  rendered  impossible,  and  fluids  introduced 
are  ejected  through  the  nose  and  mouth,  so  that  the  patient  can  neither 
be  fed  in  the  usual  way  nor  by  the  stomach  pump.  During  the  paroxysm 
the  action  of  the  inspiratory  preponderates  over  that  of  the  expiratory 
muscles,  so  that  the  act  of  coughing  is  rendered  impossible,  and  mucus 
accumulates  in  the  bronchi.  In  severe  paroxysms  the  chest  becomes 
fixed  ;  the  countenance  is  livid  ;  the  eyes  are  suffused  ;  the  patient  foams 

Fig.  93. 


Taken  from  the  okiginal  painting  by  Sir  Charles  Bell.    (From  Spence's  "Surgery"). 


at  the  mouth ;  and  he  is  tormented  with  a  feeling  of  dread  and  suffoca- 
tion. Arrest  of  respiration  may  sometimes  be  caused  by  spasm  of  the 
glottis ;  but,  as  a  rule,  it  is  the  result  of  spasm  of  the  thoracic  muscles 
and  diaphragm.  In  the  intervals  respiration  is  only  slightly  changed 
in  freciuency,  but  it  is  accompanied  by  a  painful  sensation  of  increased 
resistance,  requiring  effort.  Motor  paralysis  is  a  rare  symptom  of 
tetanus.  Rose  observed  paralysis  of  the  muscles  of  one  side  of  the 
face  in  two  cases,  and  in  one  of  them  the  tetanus  was  caused  by  a  deep 
wound  over  the  upper  jaw,  so  that  the  lesion  was  situated  in  the  area  of 
distribution  of  the  facial  nerve.  Similar  cases  have  been  recorded  by 
others.  General  muscular  weakness,  and  paralysis  of  certain  groups 
of  muscles  are  observed  as  terminal  phenomena,  and  strabismus  is, 
according  to  Wunderlich,  a  precursor  of  death. 

The  sensory  disturbances  in  tetanus  are  such  as  are  usually  produced 
by  intense  muscular  cramp  in  the  muscles  of  the  calf.     Some  observers 


SPINO-NEURAL    SPASMS.  317 

liave  noticed  an  increase  of  the  sensibility  to  pain  independently  of  the 
spasms,  while  at  other  times  the  acuteness  of  the  senses  of  touch  and 
temperature  may  be  diminished.  Pargesthesife,  such  as  numbness, 
tickling,  and  tingling,  have  occasionally  been  observed.  Pain  at  the 
epigastrium,  piercing  through  to  the  back,  is,  according  to  some  authors, 
a  pathognomonic  symptom  of  tetanus.  It  is  present  during  both  the 
tetanic  paroxysms  and  the  intervals,  and  depends  most  probably  upon 
spasm  of  the  diaphragm. 

PsyeJiical  disturbance  is  generally  absent  in  tetanus.  The  mind  is 
almost  always  clear  from  the  lieginning  to  the  end  of  the  disease 
although  delirium  or  coma  may  supervene  a  short  time  before  death, 
often  due  to  the  remedies  used.  Sleeplessness  is  one  of  the  most 
troublesome  symptoms  of  acute  cases  of  tetanus,  and  even  in  subacute 
cases  sleep  is  only  obtained  at  broken  intervals.  The  spasms  cease 
during  sleep  and  the  narcosis  of  opium  or  chloroform.  The  skin  is  hot 
and  bathed  in  perspiration,  having  a  peculiar  pungent  smell,  while  the 
surface  may  be  covered  by  sudamina  as  in  other  cases  of  profuse  sweat- 
ing. In  the  majority  of  cases  the  temperature  ranges  from  101°  F.  to 
103°  F.,  and  may  even  rise  suddenly  to  105°  F.  in  cases  which  re- 
cover, although  it  is  not  maintained  long  at  this  level  except  in  fatal 
cases.  In  many  cases  there  is  hyperpyrexia  immediately  before  death, 
the  temperature  rising  to  108°  F.  or  even  112°  F.,  and  it  may  continue 
to  rise  for  some  hours  after  death. 

The  pulse  may  remain  normal  during  the  first  stage  of  tetanus,  but 
there  is  a  considerable  increase  in  its  frequency  during  the  tetanic 
seizure,  and  in  the  last  stage,  especially  Avhen  there  is  elevation  of  tem- 
perature, it  may  beat  as  often  as  180  in  a  minute.  Listen  observed  in 
a  case  of  amputation  during  tetanus  the  vessels  so  contracted  that  not  a 
drop  of  blood  had  escaped. 

The  daily  quantity  of  urine  passed  in  tetanus  is  usually  below  the 
average  in  health;  the  reaction  is  strongly  acid;  the  specific  gravity  is 
high ;  and  there  is  generally  an  abundant  deposit  of  urates  on  cooling. 
Sugar  in  the  urine  in  tetanus  was  first  discovered  by  Demme,  and  its 
presence  has  since  been  detected  by  others.  Senator  found  that  the 
excretion  of  nitrogen  was  not  increased  in  tetanus  as  compared  with 
the  amount  excreted  by  a  person  fasting.  He  also  states  that  the  crea- 
tinine is  not  increased.  There  may  be  retention  of  urine,  caused  prob- 
ably by  spasm  of  the  sphincter,  while  at  other  times  dribbling  may 
occur  during  the  paroxysm.  The  bladder  is,  however,  never  affected 
to  so  great  an  extent  as  it  is  in  acute  spinal  meningitis.  Spasm  of  the 
sphincter  ani  is  often  present,  as  is  proved  by  the  difficulty  of  intro- 
ducing an  enema  pipe. 


31^  SPASMODIC    DISOKDEKS. 

The  general  liealth  of  the  patient  suffers  greatly  during  the  course  of 
the  disease.  The  distorted  position  of  the  body,  the  persistent  sleep- 
lessness, the  difficulty  of  respiration,  and  the  impossibility  of  swallowing 
combine  to  render  the  state  of  the  patient  extremely  distressing.  The 
bowels  are  constipated,  the  tongue  is  generally  coated,  a  tenacious  viscid 
saliva  accumulates  in  the  mouth,  and  the  patient  may  be  excessively 
hungry  and  tormented  with  thirst,  yet  can  swallow  neither  food  nor 

drink. 

The  intensity  of  the  disease  is  variable.  The  symptoms  in  slight 
cases  may  consist  only  of  trismus  and  some  stiffriess  of  the  neck  ;  in 
other  cases  they  develop  rapidly  and  prove  fatal  in  a  few  days,  or  occa- 
sionally in  a  few  hours  from  the  commencement.  Death  may  take 
place  during  a  paroxysm  from  asphyxia  caused  by  respiratory  spasm ; 
from  sudden  arrest  of  the  heart's  action  :  or  from  a  gradual  cessation  of 
the  heart's  action  during  a  paralytic  stage. 

In  cases  of  recovery  the  convulsive  attacks  become  lighter  and  less 
frequent,  but  a  considerable  degree  of  muscular  rigidity  persists  long 
after  the  paroxysms  have  disappeared.  Recovery  takes  place  in  from 
one  to  eight  weeks,  or  even  longer,  and  a  certain  degree  of  weakness 
and  stiffness  may  remain  in  the  muscles  for  a  long  time. 

In  the  tetanus  of  strychnia  the  masticatory  muscles  are  rarely  attacked 
first,  and  may  possibly  escape  altogether ;  the  symptoms  are  well  marked 
at  the  commencement,  and  reach  their  full  development  in  a  few  minutes: 
opisthotonos  is  a  very  early  symptom.  There  are  usually  intervals  of 
complete  intermission ;  and  death  occurs  commonly  in  three  hours,  or 
else  recovery  is  very  rapid. 

c.   Tetany  (Tetanilla). 

Etiology. — Tetany  occurs  most  frequently  between  the  ages  of  seven- 
teen and  thirty  years,  but  it  is  not  unfrequent  in  children  from  the 
fourth  to  the  sixth  years  of  age.  Amongst  the  predisposing  causes  of 
the  affection  may  be  mentioned  disordered  menstruation,  the  puerperal 
state,  and  pregnancy,  and  persons  are  particularly  liable  to  be  attacked 
at  the  age  of  puberty.  Tetany  has  sometimes  been  observed  as  one  of 
the  sequelae  of  typhoid  and  other  fevers,  and  either  obstinate  constipa- 
tion or  exhausting  diarrhoea  appears  to  predispose  to  the  disease,  while 
it  is  probable  that  many  cases  are  of  rheumatic  origin.  Of  the  existing 
causes  the  most  frequent  are  exposure  to  cold,  fright  or  other  emotional 
disturbance,  Avhile  it  may  occasionally  occur  as  an  epidemic  amongst 
girls  at  school. 


SPINO- NEURAL    SPASMS.  ::;i9 

Symptoms. — The  affection  generally  begins  by  tingling  and  feelincrs 
of  heat  and  cold  in  the  hands,  or  by  decided  pains  in  the  forearm  and 
hand  or  in  the  calves  of  the  legs.  Soon  afterwards  the  fingers  feel  stiff" 
and  after  a  time  this  feeling  increases  to  the  decided  spasm  which  consti- 
tutes the  chief  feature  of  the  disease.  The  spasm  occurs  in  paroxysms, 
each  of  which  begins  with  rigidity  of  the  hands  and  fingers  ;  the  thumb 
is  strongly  adducted ;  the  fingers  are  approximated  and  flexed  at  the 
metacarpo-phalangeal  and  often  extended  at  the  phalangeal  joints ;  and 
the  palm  is  made  hollow  by  the  approximation  of  its  outer  and  inner 
borders,  so  that  the  hand  assumes,  as  Trousseau  remarks,  the  peculiar 
conical  form  which  the  accoucheur  gives  to  it  when  about  to  undertake 
the  operation  of  turning.  At  other  times  the  second,  third,  and  fourth 
fingers  are  strongly  flexed  at  the  phalangeal  as  well  as  the  metacarpo- 
phalangeal articulations,  while  the  index-finger  is  only  slio-htly  flexed 
and  all  the  fingers  are  firmly  applied  to  the  thumb,  while  the  hand  is 
usually  strongly  flexed  at  the  wrist  and  directed  to  the  ulnar  border, 
although  occasionally  it  is  hyper-extended.  The  different  positions 
assumed  by  the  fingers  and  thumb  may,  indeed,  be  imitated  by  a  pow- 
erful faradic  excitation  of  the  ulnar  nerve,  or  by  a  simultaneous  excita- 
tion of  the  ulnar  and  median  nerves.  When  the  spasm  extends  upwards 
the  upper  arms  are  strongly  adducted,  and  the  forearms  are  semi-flexed 
and  are  thus  crossed  upon  the  epigastrium.  The  spasms  frequently 
extend  to  the  lower  extremities ;  the  toes  are  then  drawn  towards  one 
another  and  strongly  flexed ;  the  sole  is  hollowed  out  in  the  same  man- 
ner as  the  hand ;  the  dorsum  of  the  foot  is  strongly  arched ;  the  heel 
is  drawn  strongly  upwards  by  the  contracted  muscles  of  the  calf:  and 
the  lea;  and  thio;h  are  in  a  state  of  rigid  extension. 

From  the  extremities  the  spasm  extends  to  other  portions  of  the 
body,  but  it  is  only  very  rarely  that  a  large  portion  of  the  muscles  of 
the  body  is  simultaneously  attacked,  although  in  aggravated  cases 
the  spasm  may  invade  the  abdominal  muscles  and  the  bladder,  as  well 
as  the  muscles  of  the  face,  eyeballs,  tongue,  jaws,  neck,  and  larynx. 
Extreme  and  dangerous  symptoms  may  occasionally  be  caused  by  spasm 
of  the  muscles  of  respiration,  including  the  diaphragm. 

During  the  continuance  of  the  spasm  the  affected  muscles  feel  hard, 
tense,  resisting  to  passive  movements,  and  although  the  degree  of  con- 
traction undergoes  considerable  variations  during  the  attack,  yet  the 
muscles  never  become  entirely  relaxed.  Each  paroxysm  may  last  for 
a  few  minutes  or  a  quarter  of  an  hour  only,  but  in  some  cases  it  may 
continue  for  some  hours ;  its  violence  then  gradually  abates,  but  a 
painful  feeling  of  fatigue  and  a  certain  amount  of  rigidity  of  the  mus- 
cles are  generally  felt  for  some  time  after  the  active  spasm  has  ceased. 


y-jJO  SPASMODIC    DISORDERS. 

After  u  variable  period  of  time  the  paroxysms  recur,  and  although  the 
interval  between  them  may,  in  some  cases,  extend  over  some  days  or 
even  weeks,  yet  it  is,  as  a  rule,  only  a  feAV  hours  in  duration,  and  the 
attack  then  recurs  several  times  in  the  same  day.  In  severe  cases  the 
attacks  may  follow  one  another  so  rapidly  that  the  patient  only  remains 
free  from  spasm  for  a  few  minutes  at  a  time.  Erb  found  a  great  in- 
crease of  the  electrical  excitability  in  the  nerves  of  the  extremities 
which  supplied  the  affected  muscles,  while  the  galvanic  irritability  of 
the  nerve  was  not  only  increased,  but  a  tetanic  contraction  was  also 
obtained  by  a  feeble  current  during  cathodal  closure  and  even  with 
anodal  opening. 

The  attacks  are  preceded  and  accompanied  by  tingling,  formication, 
numbness,  and  other  abnormal  feelings,  while,  in  addition  to  the  pain 
felt  in  the  tense  muscles,  a  tearing  sensation  is  experienced  in  the 
course  of  some  of  the  nerve  trunks.  The  sense  of  touch  is  impaired, 
and  the  patient  foils  to  appreciate  the  size  and  hardness  of  objects 
grasped,  which  feel  as  if  they  were  wrapped  in  some  thick  material, 
and  when  the  lower  extremities  are  affected  the  subject  feels  as  if  he 
■were  Avalking  on  carpet.  The  paroxysms  of  tonic  spasm  are  said  by 
Trousseau  to  be  preceded  and  accompanied  b}^  loss  of  muscular  power  : 
'•movements  of  extension,"  he  says,  ''are  not  the  only  ones  abolished 
by  the  convulsive  contraction  of  the  muscles  ;  those  of  flexion  are 
equally  so.  The  fingers,  for  instance,  Avhen  half  flexed,  no  longer  obey 
the  will,  and  the  patient  cannot  close  them  further,"  and  Buzzard  has 
made  a  similar  observation.  The  joints,  especially  the  small  joints  of 
the  hand,  may  be  red,  swollen,  and  painful,  and  during  the  acme  of  the 
attack  the  body  may  be  bathed  in  perspiration,  so  that  the  patient  may 
seem  to  be  affected  with  acute  rheumatism,  and  this  appearance  has, 
indeed,  led  many  pathologists  to  believe  that  the  disease  is  of  rheumatic 
origin.  Disorder  of  the  general  health,  although  frequently  present  as 
predisposing  to  tetany,  does  not  appear  to  be  an  essential  ])art  of  the 
disease ;  but  in  severe  cases  a  certain  degree  of  fever  may  be  present, 
and  the  patient  may  complain  of  headache,  giddiness,  and  humming 
noises  in  the  ears.  The  mental  faculties  are  ahvays  unimpaired,  except 
in  those  severe  and  exceptional  cases  in  Avhich  the  respiratory  troubles 
become  so  aggravated  that  the  patient  is  threatened  with  asphyxia. 

The  symptoms  of  tetany  generally  appear  suddenly  on  exposure  to 
one  of  the  exciting  causes  of  the  affection.  Such  paroxysm  is  generally 
of  short  duration,  but  the  attack  is  liable  to  recur  for  a  period  of  weeks 
or  even  months.  The  disease  almost  always  terminates  favorably, 
although  a  case  is  mentioned  by  Trousseau  which  terminated  fatally 
from  respii'atory  spasm. 


SPIXO-NEUEAL    SPASMS.  321 


8.  Myopathic  SPAS.Mr 


a.  Local  Myopathic  Spasviis. 

A  large  number  of  spasms  are  caused  by  local  disease  of  the  affected 
muscles.  The  stiffness  which  accompanies  muscular  rheumatism,  and 
the  temporary  spasm  of  the  muscles  of  the  neck  which  is  caused  b\ 
exposure  to  cold,  are  examples  of  a  local  affection  of  the  muscles, 
although  it  is  possible  that  even  in  these  affections  the  intra-muscular 
nerve-endings  may  take  a  chief  part  in  the  production  of  the  spasm. 

h.   General  Myopatlik  Spasms  {Thomsens  Disease). 

Etiolony. — This  disease,  which  was  first  described  by  Thomsen,  who 
is  himself  a  sufferer,  is  often  inherited,  and  may  appear  in  several 
members  of  the  same  family,  as  well  as  in  successive  generations.  In 
all  cases  in  which  a  decided  hereditary  tendency  to  the  disease  was 
manifested  the  symptoms  appeared  in  early  infancy,  but  in  other  cases 
the  characteristic  spasm  did  not  appear  until  from  the  fifth  to  the  tenth 
year  of  age.  The  exciting  causes  are  any  slight  injury,  sucli  as  a  fall 
from  a  carriage,  which  is  accompanied  by  a  severe  fright. 

SynqJtonis. — The  most  characteristic  symptom  of  this  affection  is  a 
peculiar  stiffness  and  rigidity  of  the  muscles  on  voluntary  movement, 
which  may  increase  to  a  persistent  tohic  spasm  which  prevents  all 
intended  actions.  When  the  patient  performs  a  voluntary  movement 
the  muscles  contract  slowly  at  first,  but  when  the  contractions  are  once 
begun  they  persist  for  a  long  time  and  only  terminate  very  gradually, 
so  that  patients  cannot  readily  let  go  articles  they  have  once  seized. 
The  spasms  are  increased  by  cold,  during  the  incubation  stage  of  fevers, 
after  severe  and  exhausting  muscular  exertion,  and  by  emotional  dis- 
turbances. The  stiffness  is  also  increased  by  rest,  and  the  patient  ex- 
periences great  difficulty  in  beginning  any  voluntary  action,  but  when, 
by  a  great  effort,  the  intended  movement  is  once  begun,  it  is  effected 
with  increasing  freedom,  and  when  the  body  becomes  Avarm  by  exercise 
the  actions  of  the  patient  are  scarcely  to  be  distinguished  from  those  of 
healthy  persons.  The  muscles  are  well  developed  or  even  hypertrophied, 
the  electrical  reactions  are  normal  or  only  slightly  diminished,  Init  a 
tetanic  contraction  is  more  readily  obtained  than  in  health.  The  nmscles 
of  the  extremities  are  always  affected  with  the  spasm ;  in  many  cases 
the  erector  spinse  are  implicated,  so  that  the  patient  suffers  from 
spasmodic  lordosis ;  the  movements  of  the  tongue  are  often  interfered 
with,  givino-  rise  to  difficulties  of  articulation  ;  the  muscles  of  the  neck 

21 


322  SPASMODIC    DISORDERS. 

are  sometimes  also  aifectecl,  so  that  on  rotation  of  the  head  it  is  liable  to 
be  fixed  for  some  time  in  a  distorted  position  :  and  in  some  cases  the 
patient  experiences  difficulty  in  opening  his  mouth  owing  to  spasm  of 
the  masticatory  and  lower  facial  muscles,  while  in  a  case  reported  by 
Ballet  and  INIarie  the  patient  observed  at  one  time  of  his  life  that  when 
he  looked  upwards  his  eyes  became  fixed  and  he  experienced  consider- 
able difficulty  in  bringing  them  to  the  horizontal  position.  In  one 
reported  case  the  phenomena  of  this  disease  coexisted  with  all  the  char- 
acteristic symptoms  of  pseudo-hypertrophic  paralysis.  There  are  no 
sensory  disorders  in  this  disease,  but  these  patients  are  liable  to  suffer 
from  attacks  of  giddiness.  Passive  movements  of  the  limbs  do  not  pro- 
voke muscular  tension,  and  the  tendon  reactions  are  normal.  The 
patients  are  irritable,  suspicious,  and  reserved,  Avhile,  as  a  rule,  tliey 
are  morbidly  sensitive  with  regard  to  their  condition. 


CHAPTER    lY. 

SPASMODIC  DISORDERS  [continued). 

II.  CEREBRO-SPINAL  SPASMS. 

Inflammation  in  or  near  the  pyramidal  tracts  in  their  course  through 
either  the  brain  or  spinal  cord  gives  rise  to  spasmodic  jerkings  of  the  limbs, 
but  in  such  cases  paralysis  is  soon  established.  The  paralysis  caused 
by  disease  of  these  tracts  is  attended  by  muscular  tension  and  contrac- 
tions, but  these  symptoms  will  be  subsequently  described  under  the  name 
of  the  spasmodic  paralyses.  In  post-hemiplegic  chorea  and  athetosis, 
clonic  spasm  is  present  unaccompanied  by  much  paralysis,  but  both 
these  affections  are  preceded  by  an  attack  of  hemiplegia,  and  they  will 
be  more  conveniently  described  along  with  the  spasmodic  paralyses. 
There  now  remain  for  consideration  the  spasms  caused  by :  1,  organic 
disease ;  and  2,  by  functional  disease  of  the  cortex  of  the  brain. 

1.  Spasms  from  Organic  Disease  of  the  Cortex  of  the  Brain 
(Monospasms  and  Unilateral  Convulsions). 

Organic  disease  of  the  cortex  of  the  brain  gives  rise  to  attacks  of 
spasm  which  may  be  limited  to  one  limb  or  to  one  side  of  the  head 
(monospasm),  or  which  begin  in  one  limb  or  the  side  of  the  head 
(protospasm),  and  extend  to  the  other  limb  or  to  the  one  side  of  the 
head,  and  to  half  the  body  or  to  both  sides  of  the  body.  The  charac- 
teristics of  these  spasms  are  that  they  are  gradual  in  their  appearance 
and  deliberate  in  their  progress,  and  that  they  are  not  attended  by  loss 
of  consciousness,  or  the  spasm  begins  before  the  patient  becomes  un- 
conscious, so  that  he  is  afterwards  able  to  describe  a  motor  aura. 
Another  characteristic  of  these  convulsions  is  that  an  attack  is  followed 
by  a  transitory  or  permanent  paralysis  of  the  affected  muscles.  The 
clinical  varieties  of  unilateral  convulsions  may  be  divided  into — (1) 
crural,  (2)  brachial,  (3)  facial,  (4)  oculo-motor,  and  (5)  masticatory 
monospasm  or  protospasm. 


324 


SPASMODIC    DISOKDEES. 


(1)  Crural  Monospasm  or  Protospasm. 

In  crural  monospasm  the  spasm  is  limited  to  tlie  leg,  while  in  proto- 
spasm it  begins  in  the  leg,  often  in  the  toes,  and  ascending  to  the  muscles 
of  the  trunk  the  arm  is  next  attacked,  and  the  face  last.  The  spasm 
extends  to  a  greater  or  less  extent  to  both  sides  when  it  affects  muscles 
which  are  bilaterally  associated.  In  a  case  of  crural  protospasm  which 
was  recenth^  under  my  observation  the  spasm,  which  began  in  the  toes 
of  the  left  foot,  affected  the  abdominal  and  thoracic  muscles  on  both 
sides,  but  was  wholly  limited  to  one  side  in  the  extremities,  while 
the  muscles  of  the  face  were  not  much  affected.  In  the  same  case  the 
spasm  of  the  arm  began  in  the  muscles  of  the  shoulder,  and  descended 
gradually  to  those  of  the  hand.  The  tendon  reactions  were  exaggerated 
on  the  side  affected  with  spasm,  and  a  certain  degree  of  permanent 
hemiplegia  existed,  the  paralysis  being  most  marked  in  the  left  leg,  which 
was  the  part  in  which  the  spasm  always  began.  Several  cases  of  crural 
monospasm  and  protospasm  have  been  reported  in  Avhich  a  post-mortem 
examination  was  obtained,  and  the  lesion  has  always  been  found  in  or 
near  the  upper  part  of  the  ascending  parietal  convolution,  the  superior 

Fig.  94. 


parietal  lobule,  and  the  paracentral  lobule.  Bourneville  describes  a  case 
of  the  hemiplegia  of  infancy,  in  which  the  convulsions  began  by  tremors 
or  twitching  in  the  left  or  paralyzed  leg.  The  cortex  of  the  right 
hemisphere  was  found  atrophied  in  front  of  the  fissure  of  Rolando,  the 
superior  half  of  the  ascending  frontal,  the  posterior  extremities  of  the 
first  and  second  frontal  (Fig.  94),  and  the  whole  extent  of  the  para- 
central lobule. 

(2)  Brachial  Monospasm  or  Protospasm. 

In  brachial  monospasm  the  convulsions  are  limited  to  the  arm,  while 
in  protospasm  they  begin  in  the  arm,  the  face  is  next  attacked,  and  the 


C  E  R  E  B  R  O  -  S  P I X  A  L    SPASMS. 


825 


leg  last.  The  spasms  often  begin  in  the  small  muscles  of  the  hand  and 
gradually  ascend  to  those  of  the  shoulder,  this  being  the  opposite  order 
to  that  followed  by  the  spasms  when  the  convulsions  begin  first  in  the 
lower  extremity.  A  case  of  brachial  protospasm  has  been  recorded  by 
Dr.  Dreschfeld  in  which  the  attack  began  "by  sudden  clenching  of  the 
fist,  flexing  of  the  wrist,  and  pronation  of  the  forearm  on  the  left  side, 
the  corresponding  angle  of  the  mouth  being  at  the  same  time  drawn 
downwards."  At  the  autopsy  the  dura  mater  was  found  adherent  to 
the  brain  on  the  right  side  over  the  greater  part  of  the  ascending 
parietal  convolution  and  the  supra-marginal  lobule  (Fig.  95).     Several 

Fig.  9-1. 


other  cases  of  brachial  protospasm  with  post-mortem  examinations  are 
on  record,  and  the  lesion  has  always  been  found  in  or  near  the  ascending 
parietal  and  frontal  convolutions.  In  a  case  recorded  by  Dr.  Hughlings- 
•Jackson  the  spasm  began  in  the  shoulder  and  went  down  the  arm,  and 
in  this  case  a  tumor  was  found  in  the  posterior  extremity  of  the  first 
frontal  where  it  joins  the  ascending  frontal  convolution.  When,  how- 
ever, the  spasm  begins  in  the  hand  the  lesion  is  situated  near  the  lower 
end  of  the  fissure  of  Rolando. 

(3)  Facial  Monospasm  or  Protospasm. 

In  facial  monospasm  the  convulsion  is  limited  to  the  muscles  of  the 
face,  while  in  protospasm  it  begins  in  them,  extends  next  to  the  arm, 
and  attacks  the  leg  last,  if  at  all.  In  the  reported  cases  of  facial  pro- 
tospasm, with  post-mortem  examination,  the  lesion  has  always  been 
found  in  the  cortex  in  the  inferior  part  of  the  ascending  frontal  and 
parietal  convolutions  upon  a  level  with  the  posterior  part  of  the  third 
frontal  convolution.  The  case  of  a  French  soldier,  for  example,  is 
reported  by  Hitzig,  who,  two  months  after  a  bullet  wound  on  the  right 


326 


SPASMODIC    DISOEDERS, 


side  of  the  head,  suffered  from  clonic  spasms  followed  by  paralysis  of 
the  left  side  of  the  face  and  tongue.  An  abscess  was  found  in  the 
cortex  of  the  right  hemisphere,  situated  in  the  inferior  part  of  the 
ascending  frontal  on  a  level  with  the  third  frontal  convolution. 

(4)  Oculo-motor  Ilonosjyasm  or  Frotospasm. 

Many  cases  of  unilateral  epilepsy  begin  by  a  conjugate  deviation  of 
the  eyes  and  rotation  of  the  head  and  neck,  the  eyes  and  head  being 
directed  towards  the  side  affected  by  spasm.  In  some  cases  the  patients 
are  able  to  give  an  accurate  description  of  the  head  being  forcibly 
twisted  to  one  side,  but  in  other  cases  they  state  that  the  attack  is 
ushered  in  by  an  apparent  rotation  of  surrounding  objects,  this  feeling 
being  the  subjective  correlation  of  the  rotation  of  the  eyeballs  and  head. 
A  case  has  been  reported  by  my  friend  Dr.  Thomson,  of  Oldham,  in 
which  the  eyeballs  were  persistently  rotated  towards  the  right  (Fig.  06) 

Fig.  96. 


by  a  spiculum  of  bone  which  projected  towards  the  cortex  of  the  brain 
near  the  angular  gyrus  of  the  left  side  from  a  depressed  portion  of  the 
skull  over  the  infero-postero-parietal  area.     On  removal  of  this  spiculum 


CEREBEO-SPIXAL    SPASMS.  327 

of  bone  by  means  of  an  operation  the  rotation  of  the  eyeballs  almost 
immediately  ceased. 


(5)  3Iasticatori/  ^lonospasm  or  Protospasm. 

Masticatory  spasm  from  cerebral  disease  is  not  very  common,  but 
several  cases  are  now  recorded.  Lepine  has  reported  a  case  of  apo- 
plexy in  which  the  masticatory  muscles  Avere  in  a  state  of  persistent 
spasm  up  to  the  time  of  death.  At  the  autopsy  the  chief  lesion  Avas 
found  to  consist  of  a  hemorrhagic  focus  which  occupied  the  claustrum, 
external  capsule,  and  lenticular  muscles  of  the  right  hemisphere,  and 
had  separated  from  the  white  substance  a  portion  of  the  gray  matter  of 
the  Island  of  Reil,  and  of  the  inferior  part  of  the  ascending  frontal 
convolution  the  latter  Ijeing  the  part  in  which  Ferrier  places  the  centre 
for  the  movements  of  the  jaws.  Cases  in  which  trismus  was  caused  by 
disease  in  or  near  the  cortex  of  the  brain  have  also  been  recorded  by 
Petrina,  Seeligmliller,  Senator,  and  Oulmont  and  Charcot. 


2.  Spasmodic  Affectioxs  from  Functional  Disease  of  the 
Cortex  of  the  Brain. 

a.  Epilepsy. 

Etiology. — A  hereditary  taint  may  be  distinctly  traced  in  rather 
more  than  one-third  of  all  cases  of  epilepsy,  but  a  neurotic  constitution 
is  met  with  in  a  much  larger  number  of  cases.  The  disease  appears  to 
be  transmitted  rather  more  frequently  through  the  mother  than  the 
father,  and  the  female  sex  is  rather  more  frequently  attacked  than  the 
male  sex.  With  regard  to  age  Dr.  Gowers  found  that  out  of  1450 
cases  analyzed  by  him  the  disease  began  in  29  per  cent,  under  ten  years 
of  age;  in  4(3  per  cent,  between  ten  and  twenty  years ;  in  lo.T  per 
cent,  between  twenty  and  thirty  years ;  in  6  per  cent,  between  thirty 
and  forty  years ;  in  2  per  cent,  between  forty  and  fifty  years ;  and  in 
IJ  per  cent,  above  fifty  years.  Anaemia,  chlorosis,  scrofula,  rickets, 
chronic  alcoholism,  and  chronic  lead-poisoning,  appear  to  beget  a  certain 
instability  of  the  nervous  system  which  predisposes  to  the  production 
of  epilepsy. 

The  exciting  causes  of  epilepsy  are  profound  emotional  disturbance, 
intestinal  irritation  from  the  presence  of  worms,  overloading  of  the 
stomach,  the .  passage  of  gall-stones,  over-exertion,  sexual  excess,  ex- 
posure to  cold,  acute  febrile  diseases,  sunstroke,  injuries  to  the  head, 
and  injuries  to  the  principal  nerve  trunks. 


328  SPASMODIC    DISORDERS. 

Symptoms. — The  ■premonitory  symptoms  of  an  epileptic  attack  may 
be  divided  into  remote  and  immediate  warnings,  the  Latter  forming  the 
aurce  epilepticce.  The  remote  warnings  may  extend  over  hours  or  days 
before  the  attack ;  they  usually  consist  of  such  symptoms  as  headache, 
dizziness,  confusion  of  thought,  or  some  mental  change,  the  patient 
becomino-  depressed  or  morose,  or  excited,  lively,  and  irritable. 

Epileptic  aurce,  or  the  immediate  warning  of  the  paroxysms,  consist 
of  the  subsequent  account  which  the  patient  is  able  to  give  of  the  feelings 
he  experienced  immediately  before  the  attack.  The  aura  may  consist  of 
(a)  motor,  {h)  sensory,  (c)  vaso-motor  and  secretory,  or  (d)  psychical  phe- 
nomena. 

{a)  Motor  Aurce. — It  is  not  always  easy  to  distinguish  between  a 
motor  and  a  sensory  aura,  because  the  patient,  instead  of  describing  a 
spasm  in  objective  language,  often  describes  the  sensations  which  accom- 
pany the  spasm  in  subjective  language.  When,  for  instance,  the  con- 
vulsion begins  in  the  hand,  the  patient,  instead  of  describing  the  thumb 
as  being  drawn  into  the  palm,  says  that  he  felt  a  dragging  sensation  in 
the  thumb,  or  a  feeling  of  creeping  or  numbness  in  the  hand  which 
gradually  passed  up  the  arm.  And  when  the  convulsion  begins  in  the 
lower  extremity  the  aura  usually  begins  as  a  creeping  sensation  in  the 
big  toe  which  passes  up  the  leg  and  may  extend  to  the  arm  before  con- 
sciousness is  lost.  Conjugate  deviation  of  the  eyes  and  rotation  of  the 
head  and  neck,  which  frequently  usher  in  an  epileptic  attack,  are  often 
regarded  by  the  patient  as  an  apparent  rotation  of  surrounding  objects. 
At  times  patients  see  objects  recede  from  them  and  appear  smaller,  ov 
approach  them  and  become  larger,  and  these  sensations  are  pi'obably 
caused  by  variations  in  the  tension  of  tlie  muscles  of  accommodation. 
The  motor  aura  often  begins  in  the  side  of  the  face,  and  it  is  then 
described  as  a  feeling  of  "  the  face  being  drawn,"'  or  it  may  begin  in  the 
side  of  the  tongue,  and  be  described  as  a  feeling  of  something  crawling 
over  it.  In  many  cases  the  aura  consists  of  a  sudden  inability  to  speak, 
or  a  transient  aphasia.  At  other  times  it  consists  of  a  sensation  of 
shivering  or  of  trembling  in  the  muscles  of  the  back,  while  at  othei' 
times  there  may  be  a  general  tremor  or  a  jerking  of  particular  limbs, 
and  Romberg  mentions  "a  sudden  relaxation  and  loss  of  mobility '" 
as  being  sometimes  the  forerunner  of  an  attack.  In  some  cases  the 
aura  consists  of  complicated  coordinated  movements,  such  as  running 
forwards  or  backwards,  or  turning  round. 

{h)  Sensory  Aurce. — The  sensory  aura  sometimes  consists  of  a  feeling 
of  general  heat  or  cold,  while  at  other  times  it  is  distinctly  localized. 
Besides  various  sensations  such  as  tingling,  numbness,  or  pain  in  the 
extremities,  it  may  consist  of  a  localized  pain  in  any  part  of  the  head, 
or  of  a  general  feeling  of  pressure  in  the  head.     Patients  complain  of 


CEREBRO-SPINAL    SPASMS.  829 

dizziness  and  vertigo  before  an  attack,  more  frequently  perhaps  than 
any  other  form  of  aura,  but  these  symptoms  are  most  probably  but 
subjective  accompaniments  of  the  derangement  of  the  adjustments  of 
the  body  to  surrounding  objects  in  space,  which  is  caused  by  commenc- 
ing motor  discharcres. 

The  aur(E  of  the  special  sensations  may  consist  of  undeveloped  or 
crude  sensations,  or  of  more  elaborate  sensory  representations.  The 
crude  sensations  consist  of  sparks,  flashes  of  light,  and  various  colors : 
hissing,  ringing,  or  explosive  noises ;  metallic  or  other  abnormal  sensa- 
tions of  taste,  or  unpleasant  smells.  In  some  cases  the  attack  is  ushered 
in  by  sudden  blindness  of  one  or  both  eyes,  or  by  a  sensation  of  unusual 
stillness.  The  elaborate  sensory  representations  consist  of  spectral 
faces,  visions  of  beautiful  places  or  more  commonly  of  disagreeable 
objects  and  scenes,  vocal  utterances  or  strains  of  music,  and  other  com- 
plicated perceptions. 

Visceral  sensations  sometimes  constitute  epileptic  aurse,  and  probablv 
one  of  the  most  common  of  all  sensory  warnings  are  sensations  which 
are  referred  to  the  pit  of  the  stomach.  The  epigastric  aura  sometimes 
consists  of  pain,  coldness,  or  burning  at  the  pit  of  the  stomach  and  some- 
times it  is  spoken  of  as  a  vague  and  indescribable  sensation,  which  ascends 
to  the  throat  and  causes  a  feeling  of  choking,  or  rises  to  the  head,  and 
then  immediate  loss  of  consciousness  ensues.  In  some  cases  a  feeling 
of  suffocation  constitutes  the  warning,  and  in  others  there  may  be  nausea 
with  rumblino;  in  the  bowels,  retchino;,  a  feeling  of  intense  hunger, 
bronchial  asthma,  or  palpitation  with  or  without  angina. 

(c)  Vaso-motor  aurcB  are  often  described  as  a  sensation  of  coldness 
or  numbness  in  the  fingers  and  toes,  and  the  affected  part  becomes  pale 
and  cold  to  the  touch.  At  other  times  spots  in  various  parts  of  the 
body  assume  a  red  color,  and  become  the  seat  of  feelings  of  transient 
heat.  Of  the  secretory  aurce^  an  excessive  flow  of  saliva  is  probably  the 
most  commonly  observed. 

{d)  Psyehical  aurcE  are  frecjuently  experienced  in  the  form  of  a  feeling 
of  intense  horror  or  alarm,  and  the  patient  may  look  startled,  guilty,  or 
frightened.  In  other  cases  the  patient  feels  as  if  he  were  suddenly  in 
a  strange  country,  and  in  many  cases  the  aura  is  what  Dr.  Hughlings- 
Jackson  has  named  "  a  dreamy  "  or  "voluminous  "  mental  state  similar 
to  that  experienced  by  persons  in  the  act  of  drowning,  during  which  all 
the  past  events  of  life  are  said  to  crowd  upon  the  memory. 

It  is  very  important  to  study  the  order  in  whicli  the  phenomena  of 
the  aura  succeed  one  another.  The  motor  aura  generally  begins  in  small 
muscles,  which  are  organized  for  special  actions,  and  other  muscles 
become  involved  in  the  spasm  in  a  determinate  manner,  but  the  succes- 


330  SPASMODIC    DISORDERS. 

sions  of  these  motor  plienomena  Avill  be  best  studied  in  cases  of  unilateral 
epilepsy.  A  crude  sensation  of  sight,  such  as  a  red  light,  is  often 
followed  by  a  developed  perception,  such  as  the  image  of  a  man :  a 
confused  noise  may  be  succeeded  by  strains  of  music  ;  and  a  subjective 
sensation  of  smell  may  be  followed  by  efforts  to  prevent  the  effluvia  from 
gaining  admission  to  the  olfactory  chambers,  showing  that  the  sensation 
had  become  objective.  A  visual  is  not  unfrequently  associated  with  an 
aural  sensation,  sometimes  the  one  and  sometimes  the  other  taking 
precedence.  In  some  cases  the  epigastric  aura  is  followed  by  an  emotion 
of  fear  or  of  anguish,  and  the  patient  may  have  a  facial  expression  cor- 
responding to  the  emotion. 

The  epileptic  paroxysm  may  be  divided  for  the  purposes  of  descrip- 
tion into  {a)  epilepsia  mitior  or  U  petit  mal,  {h)  epilepsia  gravior  or  le 
Jiaut  mal,  and  (<?)  epileptiform  seizures. 

(a)  Epilepsia  mitior  or  le  petit  mal  consists  of  paroxysms  of  momentary 
confusion  of  thought,  or  transitory  unconsciousness.  The  patient,  for 
instance,  may  be  attacked  while  speaking ;  he  becomes  suddenly  uncon- 
scious, there  is  a  pause,  probably  in  the  middle  of  a  sentence,  but  in  a 
few  seconds  speech  is  resumed  at  the  point  where  it  was  interrupted  and 
the  sentence  is  finished.  At  times  the  attack  may  consist  of  a  feeling 
of  fainting  with  slight  confusion  of  mind,  and,  indeed,  any  of  the 
numerous  aurse  just  described  may,  along  Avith  slight  confusion  of  mind, 
constitute  a  minor  attack  of  epilepsy.  Most  of  these  attacks  are  accom- 
panied by  minor  degrees  of  muscular  spasm.  At  the  outset  of  the 
seizure  the  countenance  becomes  ghastly  pale  ;  the  pupils  contract ;  the 
eyes  are  fixed  and  staring  or  squint ;  and  the  mouth  is  slightly  drawn ; 
or  there  may  be  partial  rotation  of  the  head  and  eyes,  chewing  move- 
ments, or  rolling  about  of  the  tongue.  An  involuntary  discharge  of 
urine  or  feces  during  the  attack  frequently  occurs.  Sometimes  the 
patient  utters  a  shriek  and  reels,  or  walks  hurriedly  round  the  room  and 
then  recovers.  At  other  times  the  patient  is  unconscious  for  a  con- 
siderable time,  but  goes  on  with  the  work  in  which  he  was  en^ajxed  as 
if  he  were  conscious.  Minor  attacks  are  very  liable  to  be  followed  by 
''  epileptic  mania." 

(6)  Epilepsia  gravior  or  le  haut  mal  may  for  the  purposes  of  descrip- 
tion be  divided  into  three  stages. 

(j)  '^^e  first  stage  is  ushered  in  by  three  prominent  symptoms  which 
occur  simultaneously  ;  namely,  loss  of  consciousness,  sudden  falling,  and 
great  pallor  of  the  face,  while  a  fourth  symptom  is  often  present  in  the 
form  of  a  loud  and  piercing  cry.  The  loss  of  consciousness  is  sudden 
and  complete,  and  every  form  of  sensibility  and  mental  operation  is 
completely  abolished.     The  patient  often  falls,  as  if  struck  by  lightning, 


CEREBRO-SPIXAL    SPASMS.  331 

either  forwards  on  his  face.  Ijackwards  on  his  occiput,  or  hiterallv,  and 
so  instantaneously  that  he  has  no  time  to  select  a  place  or  attitude,  and 
may  consec^uently  fall  into  fire,  water,  or  from  a  height.  At  other  times 
the  patient  has  sufficient  warning  of  the  impending  attack  to  enable  him 
to  sit  or  lie  down.  Pallor  of  the  flice  is  probably  always  present  at  the 
beginning  of  the  attack,  although  the  symptom  is  sometimes  so  transient 
that  it  may  pass  unobserved.  The  epileptic  cry  which  the  patient  often 
utters  immediately  l)efore  or  during  the  fall  is  loud  and  piercing  and 
alarms,  according  to  Komberg,  both  man  and  animals.  It  is  probably 
produced  by  spasm  of  the  expiratory  muscles  with  closed  glottis.  Wheia 
the  patient  falls  to  the  ground  he  remains  for  a  period  of  from  two  to 
forty  seconds  in  a  rigid  condition  caused  by  a  tonic,  although  unequal, 
contraction,  of  all  the  muscles  of  the  body.  Various  distortions  are 
thus  produced ;  there  is  conjugate  deviation  of  the  eyes  with  rotation 
of  the  head  and  neck ;  the  pupils  are  dilated  and  insensible  to  light ; 
the  countenance  is  variously  altered  ;  the  jaws  are  firmly  closed  and  the 
tongue  may  be  severely  bitten  ;  there  is  opisthotonos,  and  the  different 
segments  of  the  lower  extremities  are  extended  upon  one  another  and 
upon  the  trunk,  the  foot  being  rotated  inwards  and  the  toes  widely 
separated ;  while-  the  segments  of  the  upper  extremities  are  usually 
flexed  upon  one  another,  the  thumb  being  bent  upon  the  palm,  the 
fingers  closed,  and  the  hand  pronated.  The  respiratory  muscles  are  in 
a  state  of  tonic  spasm  and  the  breathing  is  arrested.  The  pallor  of  the 
face  is  soon  replaced  by  a  dull  red  or  dusky  hue ;  the  veins  of  the  head 
and  neck  become  greatly  distended ;  the  carotids  throb  violently,  and 
the  action  of  the  heart  is  forcible,  but  the  pulse  at  the  w^rist  is  small 
or  imperceptible. 

(jj)  The  second  stage  begins  after  a  variable  period  of  from  two  to 
forty  seconds,  and  then  the  tonic  gives  place  to  clonic  spasms  which  are 
usually  more  pronounced  on  one  side  of  the  body.  The  muscles  of  the 
foce,  tongue,  pharynx,  and  larynx  are  usually  first  affected  by  clonic 
spasm,  and  those  of  the  extremities  and  trunk  are  afterwards  invaded. 
The  patient  now  presents  a  hideous  appearance  ;  the  head  is  alternately 
drawn  laterally,  or  forward  and  backward ;  the  eyes  are  convulsively 
rotated  in  various  directions,  but  upward  and  outAvard  rotation  pre- 
dominates, so  that  the  pupils  are  hidden  and  only  the  whites  of  the  eyes 
are  visible  under  the  blinking,  half-closed  lids  :  the  face  is  variously 
distorted  ;  the  jaws  are  violently  convulsed  and  the  tongue  being  severely 
bitten,  the  blood  oozes  through  the  clenched  teeth  as  a  sanguineous  froth  ; 
the  trunk  and  limbs  are  variously  thrown  about ;  and  the  contents  of 
the  bladder,  rectum,  or  vesiculae  seminales  may  be  evacuated. 

The  venous  hyperi^mia  reaches  its  maximum  just  as  the  spasms  are 


332  SPASMODIC    DISORDERS. 

beginning  to  abate  in  severity,  and  the  skin  is  bathed  in  sweat  which 
sometimes  has  a  fetid  odor.  The  heart  beats  tumultuously,  the  carotids 
throb  ;  and  the  pulse,  if  it  can  be  felt,  is  fuller  and  more  labored  than 
during  the  period  of  tetanic  contractions.  The  pupils  are  alternately 
contracted  and  dilated  and  are  said  to  be  slightly  sensitive  to  light. 
This  stage  may  last  from  a  few  seconds  to  five  or  ten  minutes,  the  average 
duration  being  from  two  to  three  minutes. 

(jjj)  The  third  strnje  is  characterized  by  a  gradual  return  to  conscious- 
ness and  voluntary  power.  The  convulsions  either  cease  suddenly  or 
wear  off  gradually,  the  period  of  transition  being  marked  by  partial 
jerkings  of  some  muscular  groups,  or  by  a  diffused  tremor  of  the  body. 
The  patient  soon  attempts  to  change  his  position  ;  he  opens  his  eyes  and 
looks  around  him  with  a  bewildered  expression,  and  may  even  attempt 
to  speak.  The  respiratory  movements  are  now  more  natural  in  rhythm, 
although  still  somewhat  irregular;  the  pupils  are  contracted;  the  pulse 
is  quieter  and  fuller  than  in  the  previous  stage  ;  the  conjunctivae  are 
injected  and  petechiae  are  often  observed  on  the  eyelids,  forehead,  and 
temples;  the  muscles  are  relaxed  and  powerless,  and  the  patient  is 
exhausted  and  disposed  to  sleep.  The  attack  is  often  followed  by 
vomiting,  and  a  large  quantity  of  pale  urine  is  often  passed. 

(iv)  The/ow^/i  or  after  stage  is  very  variable  in  the  duration,  severity, 
and  nature  of  its  sym])toms  in  different  cases.  In  some  cases  the  patient 
recovers  in  half  an  hour  and  resumes  his  usual  occupation,  but,  as  a 
rule,  recovery  is  delayed  for  a  much  longer  period.  In  many  cases  the 
general  muscular  relaxation  is  interrupted  by  clonic  spasms,  or  fibrillary 
contractions,  and  the  patient  suffers  from  lassitude  and  stupor,  from 
which  he  is  aroused  with  difficulty,  and,  if  awakened,  he  is  peevish  and 
irritable.  The  average  duration  of  the  stupor  is  about  an  hour  when 
the  attack  occurs  during  the  day,  but  when  it  occurs  in  the  evening  or 
during  the  night  it  passes  insensibly  into  the  ordinary  nocturnal  sleep. 

Complications. — Various  mental  disturbances  are  by  far  the  most  im- 
portant of  the  complications  of  epilepsy.  The  patient  sometimes  exhibits 
marked  mental  derangement  immediately  before  as  well  as  after  the 
paroxysm,  and  a  maniacal  condition  sometimes  constitutes  the  principal 
feature  of  the  attack.  After  an  attack  of  epileptic  vertigo  a  person 
may  continue  for  some  seconds,  minutes,  or  even  hours  in  a  dull,  half 
stupid  condition.  He  may  mutter  a  few  incoherent  words  or  some  lewd 
expressions,  no  matter  how  foreign  to  his  habits;  he  may  unbutton  his 
clothes  and  expose  his  person,  urinate  in  a  public  assembly,  exhibit 
himself  naked  to  his  domestics,  or  even  walk  in  public  naked  unless 
prevented,  and  on  recovery  he  has  only  the  vaguest  recollection  of 
what   has  occurred.     These,  however,  are   a  few  of  the  minor  actions 


CEREBRO-SPINAL    SPASMS.  333 

Avhicli  may  be  done  by  individuals  subject  to  epileptic  vertio-o,  imme- 
diately after  the  attack.  The  most  motiveless  and  atrocious  crimes 
are  sometimes  committed  in  this  condition,  so  that  some  medical  jurists 
are  of  opinion  that  no  epileptic  is  responsible  for  his  actions.  Epileptics 
sometimes  have  a  Avarning  of  the  approaching  maniacal  attack  and  can 
then  caution  their  friends,  but  generally  the  seizure  is  more  or  less 
sudden.  There  is  every  variety  of  intermediate  form  between  the  milder 
and  severer  cases.  Reynolds  says  that  epileptic  mania  occurs  in  about 
one-tenth  of  all  cases  of  epilepsy,  including  the  minor  attacks  of 
epileptic  vertigo,  and  having  occurred  in  the  case  of  any  one  individual 
it  is  apt  to  recur  frequently,  especially  when  several  fits  have  followed 
in  rapid  succession.  Epileptic  delirium  is  not  always  furious  and 
dangerous.  It  may  appear  in  the  form  of  preternatural  gayety  or  illu- 
sions of  the  senses  before  the  attack,  or  during  the  intervals.  Menini:;itis 
has  been  known  to  follow  epileptic  paroxysms,  but  it  is  frequently  the 
result  of  an  injury  inflicted  by  the  fall,  and  both  apoplexy  and  permanent 
paralysis  are  rare  complications  of  idiopathic  epilepsy. 

The  fre(|uency  of  recurrence  of  the  epileptic  paroxysms  varies  within 
wide  limits,  some  patients  only  having  one  seizure  a  year,  others  having 
thousands  ;  but  Reynolds  states  that  half  the  cases  are  found  to  have  a 
rate  of  recurrence  ranging  from  one  attack  in  fourteen  to  one  in  thirty 
days.  Sometimes  the  mode  of  recurrence  is  what  has  been  termed 
"serial."  The  patient  suffers  from  two  or  more  attacks  in  a  day  and 
then  there  is  a  free  interval  of  from  one  to  several  weeks. 

Each  group  of  seizures  may  be  composed  of  from  two  to  a  hundred  or 
more  single  seizures  in  twenty-four  hours.  This  condition  may  extend 
over  a  much  longer  period,  and  Delasiauve  saw  in  a  boy  of  fifteen,  within 
one  month,  a  "  collective  seizure  "  which  was  composed  of  2500  "  frag- 
mentary seizures."  The  French  have  designated  this  condition  etat  de 
maJ  epiJeptique  (status  epilepticus),  and  Bourneville  has  recently  drawn 
attention  to  the  great  increase  of  temperature  Avhich  characterizes  this 
condition.  The  patients  lie  in  a  profound  coma,  and  the  temperature 
may  rise  to  107.6°  F.,  and  still  higher  in  fatal  cases.  In  favorable  cases 
the  temjierature  gradually  falls,  but  in  other  cases  a  subsequent  rise 
takes  place,  coma  becomes  profound,  and  the  patient  dies,  often  with 
symptoms  of  collapse  associated  with  the  formation  of  acute  "  bedsores." 

b.  Eclampsia. 

Etiology. — Convulsions  are  frequent  during  the  first  two  years  of  life, 
but  become  rare  after  the  fifth  and  exceptional  after  the  seventh  year. 
The  influence  of  hereditary  predisposition  in  the  production  of  convul- 


33i  SPASMODIC    DISOKDEKS. 

sions  is  shown  by  the  fact  that  successive  infants  of  one  family  are  liable 
to  be  attacked  with  convulsions  in  the  absence  of  any  definite  cause. 
The  children  of  parents  with  neuropathic  constitutions  are  more  liable 
to  be  attacked  than  the  children  of  healthy  parents.  All  debilitating 
causes  increase  the  tendency  to  convulsions,  and  children  suffering  from 
rickets  are  specially  lialjle  to  be  attacked :  of  sixty-five  infants  attacked 
Avith  convulsions,  Dr.  Gee  found  that  no  less  than  fifty-six  of  the  number 
were  suffering  from  rickets. 

Eclampsia  has  been  divided  into  several  varieties  according  to  the 
exciting  cause  of  the  convulsions.  These  are  («)  idiopathic,  {b)  reflex, 
(r)  febrile,  (d)  asphyxia,  (e)  urtemic,  (/)  puerperal,  and  (,</)  toxic  con- 
vulsions. 

(a)  In  idiopathic  convulsions  children  are  so  predisposed  to  these 
seizures  that  an  attack  supervenes  from  the  slightest  exciting  cause  or 
even  in  the  absence  of  any  such  cause. 

{b)  Reflex  convulsions  are  caused  by  irritation  of  the  extremities  of 
peripheral  nerves.  Amongst  the  more  usual  causes  of  irritation  are 
pricking  by  pins,  wounds  and  burns  on  the  surface  of  the  body,  reten- 
tion of  urine,  the  presence  of  a  calculus  in  the  kidney,  foreign  bodies 
in  the  external  auditory  meatus,  and  irritation  of  the  digestive  canal 
from  the  presence  of  worms  or  undigested  food,  and  of  the  gums  during 
painful  dentition. 

(f)  Febrile  convulsions  often  usher  in  severe  acute  diseases  such  as 
pneumonia  and  the  eruptive  fevers.  They  appear  to  correspond  to  rigors 
in  the  adult. 

{d)  Convulsions  due  to  asphyxia  occur  in  the  course  of  diseases  of 
the  respiratory  organs. 

{(•)  Urcernic  convulsions  in  childrofi  generally  result  from  scarlatinal 
nephritis,  and  they  may  arise  from  most  forms  of  Bright's  disease  in  the 
adult. 

(/)  Puerperal  eclampsia  is,  as  a  rule,  merely  a  form  of  uremic  con- 
vulsion. 

{g)  Toxic  convulsions  are  caused  by  such  agents  as  prussic  acid, 
nicotine,  picrotoxine,  oenanthe,  crocata,  carbonic  oxide,  and  carburetted 
hydrogen. 

Symptoms. — An  attack  of  eclampsia  cannot  be  distinguished  from  a 
true  epileptic  seizure,  and  it  is  therefore  unnecessary  to  give  a  minute 
description  of  it.  Infantile  convulsions  have  been  divided  into  internal 
and  external,  the  muscles  of  the  glottis  and  the  respiratory  muscles  being 
chiefly  aff"ected  by  spasm  in  the  former  and  the  muscles  of  external 
relation  in  the  latter. 

The  symptoms  caused  by  spasm  of  the  glottis  have  already  been 


CEREBRO-SPIXAL    SPASMS.  335 

•lescribed,  aiul  we  shall  consequently  limit  our  further  remarks  to  the 
external  convulsions  of  children.  An  attack  of  eclampsia  may  occur 
either  with  or  without  premonitory  symptoms ;  but  when  present,  these 
usually  consist  of  sleeplessness  and  restlessness,  or  drowsiness  for  a  day 
or  two  before  the  attack  ;  while  immediately  before  it  the  pulse  is  often 
hard  and  wiry,  the  countenance  assumes  a  frightened  expression,  or  the 
child  starts  up  frightened  from  a  fitful  and  uneasy  sleep.  The  convul- 
sion usually  begins  by  conjugate  deviation  of  the  eyes,  and  slight  jerkin^ 
contractions  of  the  muscles  of  the  angles  of  the  mouth.  The  natural 
look  of  the  infant  is  noAv  exchanged  for  a  fixed  stare,  followed  soon 
afterwards  by  an  upward  rotation  of  the  eyeballs,  the  latter  being  in  its 
turn  followed  by  a  fixed  stare,  and  that  again  by  an  upward  rotation  of 
the  globes.  The  eyeballs  are  often  rotated  to  the  right  or  left  as  well 
as  upwards,  and  the  two  are  generally  moved  unequally,  so  that  a  con- 
siderable degree  of  strabismus  may  occur.  The  pupils  are  sometimes 
dilated,  sometimes  contracted,  and  when  they  are  completely  concealed 
by  the  superior  lids,  the  whites  of  the  eyes  being  alone  visible,  the 
countenance  assumes  a  frightful  and  characteristic  aspect. 

Clonic  spasms  of  the  facial  muscles  produce  a  series  of  grimaces  and 
contortions,  in  which  the  laljial  commissures  are  drawn  outwards,  and 
at  each  successive  jerk  a  peculiar  sucking  noise  is  made  by  the  passage 
of  air  through  the  mouth,  the  lips  being  covered  by  a  frothy,  and  often 
slightly  sanguinolent  mucus.  The  superior  lip  is  sometimes  drawn 
upwards,  so  as  to  expose  the  teeth,  and  the  countenance  then  assumes 
an  almost  savage  expression.  The  inferior  jaw  is  sometimes  agitated  by 
clonic  spasms,  while  at  other  times  there  is  trismus,  interrupted  from 
time  to  time  by  grinding  of  the  teeth.  The  head  is  usually  strongly 
retracted,  and  sometimes  rotated  to  one  side.  The  thumb  is  flexed  into 
the  palm,  and  the  fingers  are  flexed  over  the  thumb  ;  the  forearm  is 
bent  upon  the  arm  and  is  constantly  agitated  by  slight  movements  of 
semiflexion  and  semiextension ;  the  hand  is  alternately  pronated  and 
supinated ;  and  the  segments  of  the  superior  extremities  are  contorted 
into  every  imaginable  shape.  The  inferior  extremities  are  affected  in  a 
similar  manner,  although  to  a  less  degree  than  the  superior.  The 
muscles  of  the  trunk  occasionally  participate  in  the  clonic  convulsions, 
but  as  a  rule  the  trunk  is  maintained  rigid  by  tonic  contraction  of  its 
muscles.  The  contractions  of  the  muscles  of  one-half  the  body  may 
predominate  over  those  of  the  opposite  side,  and  then  the  child  is  arched 
laterally  in  such  a  way  that  he  may  be  projected  out  of  bed  by  the 
convulsion.  The  spasmodic  contractions  of  the  diaphragm  and  of  the 
muscles  of  the  larynx  produce  a  peculiar  and  characteristic  noise  when 
air  is  drawn  into  the  chest  during  inspiration.     Involuntary  evacuations 


336  h^PASMODIC    DISOKDEKS. 

occasionally  take  place  during  convulsions.  Deglutition  is  rarely  im- 
possible, although  attempts  to  get  the  infant  to  swallow  during  the  con- 
vulsion are  attended  with  danger. 

There  is  complete  loss  of  consciousness  during  the  attack,  but  reflex 
excitability  is  partially  retained.  When  the  convulsion  is  prolonged 
the  face  becomes  of  a  violet  color  and  bathed  in  perspiration ;  the  head 
is  hot  and  the  extremities  cold  ;  the  skin  is  moist ;  the  pulse  is  frequent 
and  difficult  to  count,  owing  to  jerking  of  the  tendons  ;  and  the  respira- 
tions are  accelerated,  but  stertorous  only  in  aggravated  cases. 

The  ocular  muscles  and  those  of  facial  expression  are  usually  the  fiist 
to  be  affected  with  clonic  spasm,  and  then  the  muscles  of  the  fingers  and 
forearm.  In  the  more  severe  convulsions  the  muscles  of  the  shoulders 
are  affected,  but  those  of  the  Ijack  and  loAver  extremities  are  only  impli- 
cated in  aggravated  cases.  The  great  tonic  contractions  which  form  the 
first  stage  of  the  epileptic  attack  fail  altogether  in  eclampsia.  The 
duration  of  an  attack  of  eclampsia  is  very  variable.  The  convulsions 
cease  in  some  cases  in  a  fcAv  minutes,  while  in  others  they  recur  for 
hours  or  days,  Avith  only  short  intervals  of  calm.  The  terminal  con- 
vulsions of  asphyxia  are  generally  partial,  incomplete,  and  alternate 
with  coma.  The  initial  convulsions  of  fever  are  intense  and  generalized, 
but  are  usually  limited  to  a  single  attack.  Urcemie  convulsions  are 
characterized  by  their  violence,  the  ftxMjuent  re]jetition  of  the  jiaroxysm, 
and  the  profound  coma  which  alternates  with  or  succeeds  the  spasm. 
Convulsions  caused  by  meningeal  hemorrhage  or  other  organic  lesion 
generally  assume  a  unilateral  character  and  are  followed  by  paralysis 
with  contractures,  choreiform  movements,  aphasia,  or  idiocy.  Essential 
convulsions  sometimes  terminate  fatally,  either  after  a  single  violent 
seizure,  or  after  a  series  of  seizures  which  occur  in  rapid  succession, 
death  being  caused  by  spasm  of  the  glottis  or  by  coma. 

c.  Hysterical  Spasmodic  Affections. 

Etiology. — Hereditary  predisposition  exerts  a  poAverful  influence  in 
the  production  of  hysteria,  the  transmission  being  sometimes  direct  from 
the  mother  to  the  daughter  and  at  other  times  indirect  through  in- 
heritance of  a  general  neuropathic  constitution.  Hysteria  occurs  with 
preponderating  frequency  in  the  female  sex,  and  the  first  symptoms 
usually  make  their  appearance  about  puberty,  but  it  also  occurs  in  the 
male  sex  and  is  by  no  means  unfrequently  met  with  in  children  of  both 
sexes.  All  causes  which  lower  the  nutrition  of  the  nervous  system, 
such  as  hemorrhages,  insufficient  nourishment,  impaired  digestion,  and 
anaemia,  predispose  to  hysteria.     It  is  also  frequently  induced  by  the 


CEREBRO-SPINAL    SPASMS.  337 

depressing  passions,  such  as  fear,  jealousy,  and  remorse,  as  well  as  by 
anxiety,  especially  when  combined  with  overwork.  Hysteria  may  be 
acquired,  by  those  who  are  predisposed  to  it,  by  imitation,  and  young 
susceptible  girls  are  not  unfrequently  seized  after  being  witnesses  of  an 
attack  in  another.  An  actual  epidemic  of  hysteria  may  occur  in 
public  institutions,  and  the  convulsive  diseases  of  the  middle  ages  appear 
to  have  spread  in  this  manner.  All  uterine  derangements  and  ovarian 
diseases  are  apt  to  be  attended  by  hysteria,  and  it  may  also  be  caused 
by  local  irritation  of  the  other  viscera,  such  as  intestinal  irritation  from 
the  presence  of  worms.  A  slight  contusion  or  other  insignificant  injurv 
may  cause  hysteria  in  those  who  inherit  a  strong  predisposition  to  the 
disease,  but  a  severe  injury,  such  as  a  gunshot  wound  of  a  large  nerve 
trunk,  may  induce  in  the  strongest  men  an  emotional  condition  very 
similar  to  hysteria  in  the  female. 

S'i/))ipto)ns. — The  spasmodic  affections  of  hysteria  may  be  divided 
into  (1)  general  hysterical  attacks,  and  (2)  local  spasms. 

(1)  Hysterical  Attacks 

(a)  Simple  Hysterical  Attack. — The  attack  is  preceded  by  the  sen- 
sation of  globus  along  with  a  feeling  of  suffocation,  a  painful  dragging 
in  the  extremities,  pain  and  giddiness  in  the  head,  singing  in  the  ears, 
or  darkening  of  the  field  of  vision.  It  is  often  preceded  by  a  fit  of 
crying  or  laughing,  or  a  combination  of  both ;  the  patient  suddenly 
screams  or  makes  a  spluttering  noise,  and  falls  down  in  a  state  of  ap- 
parent unconsciousness.  The  head  and  extremities  become  affected  with 
general  rhythmical  clonic  convulsions,  the  breathing  is  accelerated  and 
exaggerated,  irregular,  or  temporarily  arrested.  The  loss  of  conscious- 
ness is  more  apparent  than  real.  The  hysterical  patient  generally  hears 
what  is  said  by  those  around  her,  and  she  has  almost  always  time  to  find 
a  suitable  place  upon  Avhich  to  fall ;  she  often  throws  herself  on  a  couch 
or  reclines  on  a  sofa,  and  not  unfrequently  appears  to  bestow  some  degree 
of  attention  upon  the  propriety  and  gracefulness  of  her  attitude. 

Another  peculiarity  of  the  hysterical  attack  is  that  the  facial  expres- 
sions and  attitudes  assumed  are  not  devoid  of  meaning,  but  are  repeti- 
tions of  those  occurring  in  health  under  varying  emotions.  Sometimes 
the  expression  is  that  of  great  terror,  at  other  times  there  is  a  frown  as 
if  of  anger,  and  at  still  other  times  it  becomes  imploring  or  beseeching. 

Hysterical  attacks  rarely  last  more  than  a  few  minutes,  but  they  may 
recur  in  quick  succession,  so  that  they  seem  to  form  an  almost  con- 
tinuous paroxysm,  extending  over  a  considerable  period.  The  hysterical 
seizure  frequently  ends  in  a  fit  of  crying  and  sobbing,  there  is  no  sub- 

22 


338  SPASMODIC    DISORDERS. 

sequent  coma,  and  on  recovery  the  patient  generally  passes  a  large 
quantity  of  clear  and  limpid  urine  of  low  specific  gravity.  Hysterical 
attacks  always  occur  when  some  one  is  present  to  witness  them,  and  never 
during  sleep  or  when  the  patient  is  alone. 

(b)  Cataleptic  attacks  are  liable  to  occur  in  hysterical  patients  :  they 
are  of  variable  duration,  disappearing  sometimes  in  the  course  of  a  few 
hours,  and  being  prolonged  at  other  times,  with  slight  intermissions,  for 
a  period  of  months.  Cataleptic  rigidity  is  sometimes  limited  to  par- 
ticular hmbs ;  but,  as  a  rule,  the  whole  body  is  implicated,  and  then  all 
voluntary  movements  are  suspended  and  reflex  action  is  diminished. 
All  the  forms  of  general  sensibilit}'  are  usually  lost,  but  one  or  more  of 
the  special  senses,  especially  hearing,  may  be  retained. 

{(■)  Hysteria  in  Boys. — Boys,  at  the  approach  of  puberty,  not  un- 
frequently  suffer  from  hysterical  symptoms  resembling  those  observed  in 
the  female  sex.  Sometimes  the  symptoms  may  assume  the  form  of 
globus  along  with  attacks  of  causeless  weeping  and  sobbing ;  at  other 
times  there  may  be  partial  spasm  of  the  glottis,  a  barking  cough,  attacks 
of  dyspnoea  or  some  local  sensory  or  motor  disturbance.  l*sychical 
phenomena  often  predominate.  In  a  case  which  came  under  my  obser- 
vation, the  boy  was  sometimes  found  creeping  on  his  hands  and  knees 
and  barking  like  a  dog;  another  time  he  jumped  like  a  frog  from  the 
floor  on  to  the  table.  The  depraved  form  of  hysteria  named  chorea 
major  is  often  met  with  in  boys.  In  this  variety  of  the  disease  the 
patients  run,  dance,  jump,  or  climb  with  much  greater  readiness  and 
dexterity  than  similar  actions  could  be  performed  in  health,  or  they  may 
sing  or  recite  poetry,  even  in  a  foreign  language. 

(2)  Local  Spasms. 

In  hysteria  both  tonic  and  clonic  spasms  may  occur  in  every  muscle 
and  group  of  muscles  of  the  head,  trunk,  and  extremities.  Every  one 
of  the  spasms  already  described  as  occurring  in  the  area  of  distribution 
of  the  peripheral  motor  nerves  may  appear  in  hysteria,  but  it  is  un- 
necessary to  describe  these  in  detail.  The  facial  muscles  are  incessantly 
active  in  many  hysterical  patients,  so  that  the  countenance  has  a  restless 
and  unsettled  expression,  and,  indeed,  the  "facies  hysterica  "  constitutes 
one  of  the  main  characteristics  by  means  of  which  the  practised  physician 
is  enabled  to  diagnosticate  the  disease.  It  is  "characterized,"  accord- 
ing to  Dr.  Todd,  "  by  a  remarkable  depth  and  prominent  fulness,  with 
more  or  less  thickness  of  the  upper  lip.  There  is  also  a  fulness  and 
obviously  drooping  condition  of  the  upper  eyelids.  This  drooping  con- 
formation of  eyelids  is  at  once  a  mark  of  beauty,  and  of  that  from 


CEREBRO-SPINAL    SPASMS.  339 

■which  many  beautiful  women  suffer  very  much,  namely,  the  hysterical 
state  of  constitution." 

Spasmodic  closure  of  the  glottis  may  produce  alarming  dyspnoea,  and 
the  patients  are  liable  to  attacks  of  convulsive  laughter  and  weepino-, 
which  often  arise  apparently  in  the  absence  of  any  emotional  disturbance. 
During  hysterical  attacks  loud  screams  are  commonly  emitted,  and  in 
that  form  of  hysteria  named  chorea  major  the  patients  often  imitate  the 
cries  of  animals  by  mewing,  liarking,  or  howling.  Hysterical  patients 
often  suffer  from  a  temporary  acceleration  and  exaggeration  of  breathing 
without  there  being  any  feeling  of  embarrassed  respiration,  and  at  other 
times  they  suffer  from  temporary  spasmodic  pauses  in  the  respiratory 
rhythm.  Hiccough  and  yawning  are  frequent  and  sometimes  very  dis- 
tressing symptoms. 

The  pharyngeal  muscles  are  sometimes  spasmodically  contracted,  so 
that  swallowing  becomes  difficult  or  impossible.  Spasm  of  the  tongue 
is  not  unfrequently  associated  with  that  of  the  pharyngeal  muscles,  and 
at  every  attempt  to  move  the  organ  it  becomes  distorted  in  various  direc- 
tions, so  that  articulation  and  swallowing  become  greatly  impeded.  The 
sensation  of  choking  in  the  throat,  named  globus  hystericus^  is  supposed 
by  some  to  be  caused  by  a  spasm  of  the  oesophagus,  while  at  other  times 
the  spasm  may  be  so  persistent  as  to  resemble  organic  stricture. 

The  stomach  is  liable  to  undergo  spasmodic  contractions,  which  give 
rise  to  persistent  and  distressing  vomiting.  The  patient  vomits  almost 
immediately  after  food  is  taken,  and  the  latter  is  usually  consequently 
ejected  in  an  undigested  condition.  Some  of  the  food  is,  however, 
probably  retained,  as  the  nutrition  of  the  patient  rarely  suffers  in  pro- 
portion to  the  apparent  violence  and  persistency  of  the  vomiting. 

Irregular  peristaltic  movements  occur  in  various  parts  of  the  intestines, 
and  these  may  be  so  energetic  that  they  can  be  felt  through  the  abdominal 
wall,  and  the  patient  may  become  convinced  that  a  movable  body  is 
present  in  the  abdomen.  Spasm  of  certain  portions  of  the  intestines 
may  be  so  persistent  as  to  cause  temporary- stricture,  and  the  bowels 
above  the  constricted  portion  become  so  distended  with  gas,  as  to  give 
rise  to  what  has  been  called  a  "  phantom  tumor ;  "  or  a  real  obstruction 
of  the  bowels  may  sometimes  be  caused  by  accumulation  of  feces  behind 
the  constricted  portion.  Eructations,  borborygmi,  and  griping  pains 
may  also  be  caused  by  irregular  peristaltic  movements  of  various  por- 
tions of  the  digestive  canal. 

Spasmodic  retention  of  urine,  generally  combined  with  increased  in- 
clination to  micturate,  occurs  in  many  hysterical  patients,  and  this 
condition  is  sometimes,  but  not  always,  associated  with  a  painful  condi- 
tion of  the  genitals. 


340  SPASMODIC    DISORDERS. 

Vaginismus,  caused  by  spasm  of  the  constrictor  vaginae,  sometimes 
renders  coitus  difficult  or  impossible ;  it  is  generally  associated  with 
hyperfesthesia  of  the  vaginal  orifice,  and  the  spasm  is  induced  by  reflex 
action. 

Hysterical  patients  are  also  liable  to  suff"er  from  attacks  of  palpitation, 
and  during  these  the  pulse  is  small  and  hard  and  the  skin  pale  and 
cold,  owing  to  spasm  of  the  small  arteries  of  the  body.  Patients  suffer- 
ing from  hysteria  are  also  subject  to  fainting  fits,  and  these  are  most 
probably  caused  by  sudden  anemia  of  the  brain  from  spasm  of  its 
vessels. 

d.  Hystcro-epilepsy. 

In  hystero-epilepsy  the  patient  suffers  in  the  intervals  between  the 
attacks  from  various  hysterical  symptoms,  the  most  usual  of  which  are 
complete  or  incomplete  hysterical  hemianjvisthesia  associated  with 
ovarian  hypersesthesia.  The  paroxysm  is  always  preceded  by  an  aura, 
consisting  of  a  sensation  which  proceeds  from  the  region  of  the  hyper- 
iesthetic  ovary  and  ascends  successively  to  the  epigastrium,  throat,  and 
head,  and  on  reaching  the  last  the  patient  utters  a  loud  shriek  and  falls 
to  the  ground.  All  the  muscles  of  the  body  now  become  the  subjects 
of  tonic  spasm ;  the  head  is  retracted,  and  the  body  and  limbs  are 
arched  backwards  and  rigid ;  the  respirations  are  stertorous  and  infre- 
quent ;  and  foam,  sometimes  bloody  from  the  tongue  being  bitten, 
generally  issues  from  the  mouth.  The  tonic  stage  is  followed  by  a  few 
clonic  convulsions,  but  these  soon  cease,  and  a  state  characterized  by 
general  muscular  relaxation,  stertorous  breathing,  and  coma,  terminates 
that  portion  of  the  attack  which  resembles  the  epileptic  paroxysm. 

The  second  stage,  or  what  the  French  call  the  '■'■phase  des  grand 
mouvements,"  now  makes  its  appearance.  The  body  is  arched  back- 
Avards  in  a  state  of  opisthotonos,  or  bent  forwards  or  laterally ;  while  at 
other  times  it  is  maintained  in  a  rigid  position,  with  the  lower  extremities 
extended  and  the  upper  stretched  out.  This  stage,  according  to  Richer, 
"  consists  of  movements  Avhich  may  be  executed  with  a  certain  rhythm, 
or  in  the  most  complete  disorder,  and  often  with  excessive  violence.  In 
addition  to  screaming,  there  is  a  disposition  to  bite  and  to  tear,  and 
sometimes  the  patient  becomes  furious.  At  other  times  the  attack  of 
the  grand  movements  is  in  no  way  frightful  and  consists  almost  exclu- 
sively of  salutations,  jumping,  and  somersaults,  which  recall  to  mind 
the  performance  of  acrobats,  and  justify  the  name  of  "  attaques  de 
clownisme  "  that  has  been  given  to  it. 

The  third  stage,  or  stage  of  emotional  attitudes  {phase  des  attitudes 
passionelles),   now  appears,  and   during   its   continuance  the  patient 


CEREBRO-SPINAL    SPASMS.  3-il 

assumes  in  rapid  succession  attitudes  and  gestures  expressive  of  various 
emotions.  The  first  attitude  assumed  by  the  patient  is  usually  a  threaten- 
ing one  ;  she  raises  herself  in  a  half-sitting  posture  ;  the  brows  frown  ; 
the  fists  are  clenched ;  and  the  face  presents  an  angry  and  menacino- 
expression.  This  attitude,  however,  soon  gives  place  to  an  expression 
of  abject  fear,  which  in  its  turn  makes  room  for  a  look  of  intense  happi- 
ness and  beatitude.  But  the  expression  of  beatitude  is  also  fleetino'  in 
character,  and  is  succeeded  by  one  of  intense  voluptuousness,  followed 
by  gestures  which  lead  to  this  stage  being  called  the  phase  of  luhricity. 
Terror  now  seizes  the  patient ;  she  sees  rats  and  other  odious  animals  that 
ev^oke  from  her  passionate  exclamations  of  dread  and  disgust,  and  this  is 
followed  by  a  stage  in  which  she  appears  to  be  laboring  under  the  idea 
that  she  committed  a  great  oifence,  and  sues  for  mercy.  The  patient 
now  hears  strains  of  music,  she  looks  pleased  and  may  join  in  hummino- 
the  tune,  but  her  singing  is  soon  followed  by  weeping,  broken  bv  re- 
proaches addressed  to  her  parents  as  the  cause  of  her  misery.  This 
last  phase  constitutes  the  phase  of  recovery,  but  hallucinations  may 
persist  for  some  time.  The  patient  can  always  describe  afterwards  the 
hallucinations  to  which  she  was  subject,  and  each  of  the  attitudes  is 
found  to  have  corresponded  to  an  hallucination. 

An  attack  of  hystero-epilepsy  may  be  provoked  at  any  time  by  various 
manipulations,  such  as  suddenly  gripping  the  skin  of  the  breast  on 
both  sides,  on  a  level  with  the  fifth  rib,  and  midway  between  the  anterior 
and  posterior  boundaries  of  the  axillae.  An  attack  is  also  readily 
induced  by  pinching  a  fold  of  the  skin  of  the  sub-inguinal  region,  or  by 
slight  pressure  on  the  region  of  the  hyperiesthetic  ovary.  Sudden  and 
firm  pressure  exerted  on  the  affected  ovary,  however,  instantly  arrests 
the  paroxysm  at  any  stage.  When  such  compression  of  the  ovary  is 
made,  the  patient's  mouth  opens  Avidely,  the  tongue  is  spasmodically  pro- 
truded, and  the  convulsions  cease.  Attacks  of  hystero-epilepsy  are  not 
often  seen  in  this  country  in  the  typical  form  described  by  French 
authors. 

Hystero-epileptic  attacks  may  occur  in  series  like  epileptic  attacks, 
and  each  group  of  attacks  may  consist  of  from  several  hundreds  to  over 
a  thousand  separate  seizures,  while  group  after  group  of  these  attacks 
may  follow  each  other  day  by  day  for  weeks.  This  status  hystericus 
is,  however,  unlike  the  status  epilepticus  in  the  facts  that  the  tongue  is 
not  bitten,  that  there  is  no  elevation  of  temperature,  and  that  it  is  never 
fatal. 


342  SPASMODIC    DISOEDEES. 

e.  Catalepsy. 

Etiology. — Catalepsy  often  occurs  as  one  of  the  many  manifestations 
of  hysteria,  while  at  other  times  it  is  caused  by  chronic  cerebral  dis- 
ease,"^ such  as  softening,  tubercular  meningitis,  and  tumors.  In  some 
cases  the  cataleptic  condition  appears  to  be  premonitory  of  epilepsy, 
Avhile  in  other  cases  attacks  of  catalepsy  recur  at  certain  intervals,  and 
thus  appear  to  take  the  place  of  epileptic  seizures.  Some  cases,  how- 
ever, cannot  be  traced  to  any  external  cause,  and  then  catalepsy  may 
be  called  idiopathic  or  essential,  cases  of  this  kind  being  observed  in 
families  who  inherit  a  decided  neurotic  disposition.  The  disease  is 
most  frequently  observed  about  the  age  of  puberty,  but  it  has  been 
met  with  as  early  as  eight  years  of  age,  or  even  earlier,  and  occasion- 
ally in  advanced  life.  The  two  sexes  appear  to  be  equally  liable  to 
the  idiopathic  variety,  but  the  hysterical  is  almost  exclusively  observed 
in  the  female.  The  exciting  causes  of  idiopathic  catalepsy  are  gastric 
and  intestinal  irritation,  and  great  emotional  disturbance.  Malarial 
infection  is  said  to  have  caused  typical  attacks  of  catalepsy. 

Symptoms. — The  cataleptic  attack  is  sometimes  preceded  by  pre- 
monitory symptoms,  such  as  headache,  vertigo,  trembling  of  individual 
muscles,  and  an  undefined  sense  of  discomfort.  As  a  rule,  the  attack 
begins  abruptly ;  the  movements  of  the  patient  are  suddenly  arrested, 
it  may  be  while  he  is  speaking  or  performing  some  action  ;  the  face 
becomes  deadly  pale;  the  respirations  are  slow  and  tranquil;  the  pulse 
is  soft ;  and,  although  consciousness  is  lost,  the  attitude  of  the  patient 
at  the  time  of  the  seizure  is  retained.  The  muscles  in  action  at  the 
beginning  of  the  attack  appear  to  be  the  first  to  become  rigid,  but  in 
most  cases  the  spasm  rapidly  extends  to  all  the  voluntary  muscles, 
although  occasionally  it  is  partial  or  unilateral.  The  affected  mus- 
cles feel  firm,  and  offer  resistance  to  passive  movements  of  the  limbs, 
which  is  sometimes  so  great  as  to  amount  to  tetanic  rigidity,  but  when 
once  this  resistance  is  overcome  the  limbs,  head,  and  neck,  or  features 
may  be  placed  in  constrained  positions,  which  they  retain  for  a  com- 
paratively long  period.  After  the  first  resistance  of  the  muscles  has 
been  overcome  the  limbs  possess  a  flexibility  and  pliability,  Avhich  has 
been  compared  to  that  of  soft  wax,  and  the  condition  has  consequently 
been  named  flexihiUtas  cerea.  The  resistance  of  the  muscles  enables 
the  limbs  to  be  moulded  in  any  position  compatible  with  the  rigidity  of 
bones  and  inextensibility  of  ligaments,  and  the  constrained  attitudes  in 
Avhich  the  limbs  may  be  placed  are  maintained  without  change  during 
the  whole  course  of  the  attack.     But  even  during  the  cataleptic  condi- 


CEREBKO-SPIXAL    SPASMS.  843 

tion  the  muscular  stiffness  does  not  persist  in  its  full  intensity  for  a 
lengthened  period.  After  some  minutes  the  stiifness  diminishes  some- 
what, so  that  the  arm,  for  instance,  when  raised  horizontally  falls  lower 
by  its  own  weight,  and  the  limb  undergoes  a  slight  trembling,  indicat- 
ing the  approaching  exhaustion  of  the  muscles. 

Consciousness  is  usually  al)olished,  but  not  in  all  cases.  A  certain 
amount  of  consciousness  may  be  retained  in  the  early  stage  of  the 
attack  or  be  present  throughout,  so  that  strong  peripheral  irritation 
may  cause  pain  Avhich  will  be  remembered  by  the  patient.  Reflex 
irritability  is  sometimes  lost;  at  other  times  certain  reflex  actions,  such 
as  closure  of  the  eyelids  on  touching  the  conjunctiva,  are  retained. 
The  electric  contractility  of  the  muscles,  according  to  Benedikt,  is 
somewhat  diminished  during  the  attack,  but  soon  becomes  normal,  and 
in  a  case  observed  by  Rosenthal  the  electrical  reaction  of  the  nerves  to 
both  currents  was  perfectly  normal,  in  another  it  was  increased. 

The  organic  functions  are  not  usually  seriously  interfered  with.  The 
respiration  may  be  normal,  but  is  generally  slow  and  shallow.  The 
pulse  is  slow,  soft,  and  compressible.  The  temperature  is  generally 
lowered,  and  at  times  the  surface  of  the  body  becomes  icy  cold.  When 
the  surface  of  the  body  is  cold,  and  the  pulse  at  the  wrist  and  respiration 
are  almost  imperceptible,  the  condition  may  be  mistaken  for  real  death. 

The  attack  of  catalepsy  is  sometimes  very  brief,  lasting  only  a  few 
minutes,  at  other  times  several  hours  or  days.  Attacks  described  as 
being  very  protracted  are  in  reality  made  up  of  a  succession  of  these, 
separated  from  one  another  by  intervals  in  which  the  patients  recover 
either  wholly  or  partially.  The  seizures  sometimes  disappear  quite 
suddenly,  and  the  patients  at  once  recover  full  consciousness  and  im- 
mediately resume  the  actions  which  had  been  interrupted.  As  a  rule, 
however,  recovery  is  gradual,  patients  at  first  being  stupefied  as  if 
awaking  from  a  profound  sleep,  a  certain  amount  of  muscular  stiffness 
remaining  for  some  time,  which  renders  motion  difficult  and  slow. 

In  simple  catalepsy  no  mental  disorder  is  observed  in  the  intervals 
between  the  attacks,  but  when  it  is  merely  a  symptom  of  profound  ner- 
vous disease  the  intervals  may  be  characterized  by  the  occurrence  of 
hysterical  convulsions,  delirium,  maniacal  attacks,  and  hallucinations,  or 
the  catalepsy  may  be  associated  with  ecstasy  and  somnambulism. 

The  course  of  catalepsy  is  usually  chronic,  extending  over  many 
years.  Some  individuals  suffer  only  from  a  small  number  of  attacks 
separated  by  intervals  of  many  years.  Others,  again,  have  frequent 
periodical  attacks.  In  hysterical  catalepsy  the  slightest  external  influ- 
ence may  suffice  to  provoke  a  paroxysm.  Cataleptic  attacks  are  hardly 
ever  fatal  of  themselves. 


PA-i:  SPASMODIC    DISORDERS, 


f.   Trance. 

In  trance  the  patient  lies  for  days  together  without  eating  or  drink- 
inc',  there  is  apparent  insensibility,  and  the  pulse  and  respiration  are 
imperceptible,  but  the  limbs  remain  flexible  and  the  tonic  rigidity  of 
catalepsy  is  absent.  The  state  of  complete  insensibility  is  not,  how- 
ever, continuous,  inasmuch  as  there  occur  periods  during  which  the 
patient  may  see,  hear,  and  remember  all  that  goes  on  about  him,  and 
may  partake  of  small  quantities  of  food.  The  condition  of  the  patient 
is  not,  indeed,  unlike  that  of  a  hibernating  animal.  In  the  state  of 
trance  the  patient  usually  lies  in  a  warm  room,  Avell  covered  with 
clothing,  so  that  little  heat  is  lost  by  radiation ;  the  mental  functions 
are  in  abeyance,  indicating  that  the  molecular  changes  which  are  the 
correlatives  of  mental  actions  have  ceased,  and  all  muscular  movements 
are  suspended  with  the  exception  of  the  cardiac  contractions,  and 
slight  respiratory  movements,  and  under  such  circumstances  the  amount 
of  waste  must  be  small.  The  physician  must,  of  course,  be  on  his  guard 
against  deception  in  cases  of  trance. 

g.  Ecstasy. 

This  condition  is  closely  allied  to  trance,  the  patient  being  insensible 
to  outward  impressions  in  both.  In  ecstasy  the  mind  is  absorbed  with 
some  fixed  idea,  generally  of  a  religious  character,  and  the  patient 
becomes  oblivious  of  surrounding  events  and  objects.  The  limbs  are 
motionless,  and  often  fixed  in  maintaining  a  particular  attitude,  the 
breathing  is  slow  and  feeble,  the  pulse  is  almost  imperceptible,  the  eyes 
are  often  bright  and  animated,  and  the  countenance  has  an  expression 
of  rapture. 

h.  SomnambuUsm  and  Hypnothm. 

In  somnambulism  the  patients  appear  to  be  wholly  unconscious,  yet 
they  walk,  climb,  and  avoid  obstacles,  and  may  manifest  greater  strength, 
agility,  and  precision  of  muscular  adjustments  than  during  waking 
hours. 

Hypnotism  or  mesmerisyn  is,  as  Maudsley  remarks,  a  kind  of  artifici- 
ally induced  somnambulism.  The  subject,  who  is  probably  always  of  a 
neurotic  temperament,  is  induced  to  look  steadily  at  the  operator,  the 
latter  attracting  his  attention  by  making  a  few  gentle  "passes"  with 
his  hand.  Mr.  Braid,  of  Manchester,  directed  the  person  to  look  upon 
a  disk  or  some  bright  object  held  in  front  of  and  a  little  above  the  level 
of  the  eyes.     After  a  short  time  there  is  a  slight  tremor  of  the  eyeballs 


CEREBRO-SPINAL    SPASMS.  345 

of  the  subject,  bis  pupils  dilate,  and  be  falls  into  the  mesmeric  condi- 
tion. In  this  state  the  mental  functions  are  abolished,  and  all  the 
actions  of  the  subject  are  afterwards  determined  by  the  suggestions  of 
the  operator.  Under  the  influence  of  these  suggestions,  the  subject  mav 
sing,  recite  poetry,  and  perform  the  most  absurd  and  outrageous  actions. 
He  may  be  made  to  eat  a  raw  cabbage,  amidst  all  the  outward  sions  of 
enjoyment,  to  appease  a  suggested  hunger;  he  may  spit  out  pure  water 
given  him  to  drink  with  all  the  signs  of  disgust,  on  the  suggestion  that 
it  is  bitter  and  nauseous,  or  drink  infusion  of  wormwood  with  apparent 
relish  on  being  told  that  it  is  an  agreeable  beverage  ;  or  he  may  be  made 
to  sneeze  violently  on  being  asked  to  take  a  pinch  of  snuff  from  an 
empty  box.  Hysterical  patients  may  be  thrown  into  a  condition  of 
trance  or  of  catalepsy,  or  one  half  of  the  body  may  be  thrown  into 
trance  and  the  other  half  into  catalepsy,  by  being  made  to  look  upon  a 
brio;ht  lif^ht. 

Morhid  Anatomy  and  Physiology. — Morbid  anatomy  has  not  yet 
thrown  much  light  upon  the  nature  of  local  spasms.  These  spasms  are 
most  liable  to  occur  in  muscles  which  are  engaged  in  special  actions, 
such  as  the  facial  muscles,  the  rotators  of  the  head  and  neck,  and  the 
small  muscles  of  the  hand.  These  local  spasms  are  most  probably 
caused  by  irritation  of  some  part  of  the  reflex  loop.  The  irritation  is 
probably  sometimes  direct,  but  it  is  undoubted  that  it  is  frequently  of 
reflex  origin.  The  reflex  nature  of  these  spasms  is  well  illustrated  in 
some  cases  of  facial  tic.  When  motor-arresting  points  are  obtained  in 
such  cases  they  are  observed  not  in  the  course  of  the  facial  nerve,  but 
over  certain  points  of  the  trigeminal  nerve.  The  nature  of  these 
spasms  will,  however,  be  best  illustrated  by  a  detailed  reference  to  the 
pathology  of  the  professional  hyperkineses.  The  combinations  of 
muscular  contractions  concerned  in  writing  are  exceedingly  complex, 
but  some  of  these  combinations  are  more  special  than  others.  The 
operation  of  writing  is  divisible  into  the  acts  of  (1)  prehension  of  the 
pen,  (2)  moving  the  pen,  (3)  poising  the  hand  and  forearm.  Of  thes& 
acts  the  first  and  the  third  are  the  most  special,  and  they  are  certainly 
the  most  liable  to  be  affected  in  writer's  cramp.  The  act  of  prehension 
is  mainly  effected  by  the  muscles  of  the  ball  of  the  thumb  and  the  in- 
terossei,  and  spasm,  weakness,  and  incoordination  of  the  movements 
of  these  muscles  are  the  more  frequent  symptoms  of  the  disease. 
Poising  of  the  hand  and  forearm  is  effected  chiefly  by  the  pronators  and 
supinators  of  the  forearm,  and  as  the  hand  is  always  held  in  a  position 
in  which  gravity  aids  the  pronators,  the  most  delicate  part  in  preserving 
the  attitude  is  thrown  upon  the  supinators,  and  a  sudden  jerking  of  the 
latter  muscles  causing  the  hand  to  roll  outwards  is  not  an  unfrequent 


3J:6  SPASMODIC    DISOEDERS. 

symptom  of  the  disease.  Professional  cramps  are  doubtless  caused  by 
a  functional  or  molecular  lesion  of  some  part  of  the  nervous  mechanism 
■which  reo-ulates  the  actions  of  the  muscles  executing  the  movements 
which  are  disordered.  It  is  very  likely  that  professional  cramps  are 
sometimes  caused  in  the  same  way  as  cramp  of  the  calf  by  irritation  of 
the  intramuscular  nerve  endings,  or  the  end  ])lates  in  the  muscular 
fibres.  It  is  possible  that  at  other  times  the  seat  of  the  lesion  is  the 
mechanism  of  cells  and  fibres  in  the  anterior  gray  horns  of  the  spinal 
cord  which  regulates  the  movements  concerned  in  writing,  while  in  still 
other  cases  the  lesion  is  probably  situated  in  the  cortical  centre,  or  in 
the  course  of  the  centrifugal  conducting  paths  Avhich  connect  it  with 
the  spinal  cord.  We  should  say  that  the  chief  lesion  is  situated  in  the 
ganglion  cells  of  the  spinal  cord,  or  in  the  fibres  which  connect  them 
Avitli  the  muscles  in  all  those  cases  in  which  the  electrical  reactions  of 
the  muscles  are  diminished,  and  that  it  is  situated  either  in  the  cortex 
or  in  the  cerebral  conducting  path  above  the  spinal  level  in  all  those 
cases  in  which  the  electrical  reactions  are  increased,  especially  if  this 
increase  is  maintained  when  the  disease  is  of  long  standing. 

Saltatory  spasm  is  here  placed  amongst  the  spino-peripheral  spasms, 
because  a  case  recorded  by  Bamberger  appears  to  indicate  that  the 
excess  of  reflex  action  in  such  cases  originated  in  the  skin.  The  spasms 
are,  however,  regarded  by  Frey  as  being  caused  by  undue  tension  and 
stretching  of  the  muscles,  and  it  is,  therefore,  possible  that  some  of 
of  the  recorded  cases  are  caused  by  exaggerated  tendon-reactions.  A  few 
of  the  recorded  cases  appear  to  have  been  of  liysterical  origin,  while  in 
others  the  presence  of  contractures  shows  that  the  affection  was  caused 
by  some  form  of  lateral  sclerosis.  It  is,  indeed,  very  probable  that  very 
different  aff'ections  have  been  grouped  together  under  this  name. 

Tetanus  is  here  placed  amongst  the  spino-j)eriplieral  spasms  because 
there  can  be  little  doubt  that  increased  irritability  of  the  gray  matter 
of  the  spinal  cord  plays  a  very  important  i)art  in  the  production  of 
the  symptoms  of  idiopathic  and  traumatic  tetanus  as  well  as  of  the  tetanic 
spasms  which  are  caused  by  strychnine  and  other  poisons.  Lockhart 
Clarke  found  great  hypercemia  of  the  spinal  cord  and  its  memliranes 
as  Avell  as  foci  of  softening  in  the  gray  and  white  substance  of  the  cord 
in  cases  that  died  from  tetanus,  and  these  observations  have  been  con- 
firmed by  numerous  other  investigators.  Similar  changes  have  also 
been  found  in  the  medulla  oblongata.  It  is,  however,  po.ssible  that  the 
changes  which  have  been  discovered  were  caused  by  the  great  conges- 
tion of  the  cord  and  membranes  which  must  have  resulted  from  the 
violent  attacks  of  spasm.  Some  pathologists  believe  that  tetanic  seizures 
are  caused  by  an  increased  irritability  of  the  gray  matter  of  the  spinal 


CEREBRO-SPIXAL    SPASMS.  347 

cord  and  of  the  medulla  oblongata.  This  increased  irritability  of  the 
.spinal  centres  not  only  raises  the  irritability  of  the  i-efle.x  arcs,  but  also 
gives  rise  to  spontaneous  discharges  of  energy,  and  both  of  these  con- 
ditions are  doubtless  present  in  tetanus.  I  am,  however,  inclined  to 
believe  with  Dr.  Hughlings-Jackson  that  discharges  of  nerve  energv 
from  the  cortex  of  the  cerebellum  are  the  main  cause  of  the  paroxysms 
of  spasm  in  tetanus,  although  these  discharges  may  to  some  extent  be 
determined  by  the  instability  of  the  centres  in  the  medulla  oblongata 
and  spinal  cord.  Tetany  is  believed  by  many  authors  to  be  also  caused 
l)y  an  increased  irritability  of  the  spinal  centres,  but  pathological 
anatomy  has  not  thrown  much  light  upon  the  question.  The  theory  of 
cerebellar  discharge  is  probably  as  applicable  to  tetanus  as  it  is  to  tetany, 
Init  it  must  be  admitted  that  the  question  is  one  which  can  hardly  be 
determined  in  the  present  state  of  our  knowledge. 

Thomsen's  disease  would  appear  to  be,  according  to  the  latest  re- 
searches of  Erb,  a  primarily  muscular  disease.  If  this  view  should 
turn  out  to  be  correct,  this  disease  will  hold  the  same  relation  to  the 
spino-neural  spasms  that  pseudo-hypertrophic  paralysis  bears  to  the 
spino-neural  paralyses. 

It  has  been  found  most  convenient  to  describe  the  morbid  anatomy  of 
the  cortical  monospasms  and  protospasms  along  with  the  clinical  descrip- 
tion of  the  different  varieties  of  these  spasms.  The  most  important 
characteristic  of  these  lesions  is  that  they  are  what  Dr.  Hughlings- 
Jackson  has  called  "coarse  disease,"'  that  is,  a  disease  which  can  be 
recognized  by  the  naked  eye.  It  now  remains  for  us  to  connect  the 
morbid  changes  Avith  the  symptoms.  When  an  irritative  lesion  is  situated 
in  or  near  the  motor  area  of  the  cortex  of  the  brain  the  surrounding 
parts  are  more  freely  supplied  with  blood  and  the  gray  substance,  after 
absorbino;  a  lar^e  stock  of  nourishment,  discharges  its  accumulated 
energy  at  periodical  intervals,  thus  giving  rise  to  paroxysms  of  convul- 
sions of  the  muscles  whose  actions  are  regulated  from  that  part  of  the 
cortex.  Every  excessive  discharge  of  energy  is  followed  by  exhaustion 
of  the  motor  centres  near  the  irritative  lesion,  and  consequently  each 
convulsive  paroxysm  is  followed  by  a  transient  paralysis  of  the  affected 
muscles.  The  lesion  may  destroy  a  portion  of  the  cortex  Avhile  main- 
taining the  neighboring  portions  in  a  state  of  irritation,  and  consequently 
cortical  monospasms  are  often  accompanied  by  a  permanent  paralysis 
of  some  groups  of  muscles,  and  the  convulsive  paroxysm  always  begins 
in  the  neighborhood  of  the  paralyzed  muscles.  The  annexed  diagram 
(Fig.  97)  will  readily  explain  the  order  in  which  the  spasm  progresses 
in  the  chief  varieties  of  unilateral  convulsion.  If  the  lesion  is  situated 
near  the  longitudinal  fissure  between  the  fissure  of  Rolando  the  spasm 


348 


SPASMODIC    DISORDERS, 


will  beo-in  in  the  leg,  and  as  the  wave  of  molecular  disturbance  extends, 
the  arms  are  next  involved  and  the  i\ice  last.  If  the  lesion  is  situated 
near  the  frontal  convolution  the  spasm  will  begin  in  the  muscles  of  the 
face,  those  of  the  hand  are  next  involved,  and  those  of  the  leg  last.  If 
the  lesion  is  situated  about  the  sulcus  of  Rolando,  the  spasms  will  begin 
in  the  muscles  of  the  arm  and  hand,  those  of  the  face  are  involved 

Fig.  97. 


External  Convex  Surface  of  the  Human  Brain. 

Fissures:  R,  Fissure  of  Kolando  ;  S/,  Fissure  of  Sylvius;  pf.  Parallel  fissure  ;  ipf,  Interparietal  fissure  : 
pof,  External  parieto-occipital  fissure.  Couvobiliotis  and  Lobules :  A,  Ascending  frontal ;  B,  Ascending 
parietal  convolutions;  Fj,  Fo,  F3,  First,  second,  and  tliird  frontal  convolutions;  Pj,  Superior  parietal 
lobule  ;  Po,  Supra-marginal  gyrus  ;  P3,  Angular  gyrus  ;  0],  Oo,  O3,  First,  second,  and  third  occipital  cim- 
volutions  ;  Tj,  To,  T3,  First,  second,  and  third  temporo-sphenoidal  convolutions.  Mnlor  Centres:  ],  Move- 
ments for  rotation  of  head  and  neck ;  2,  Movements  of  the  upper  facial  muscles  ;  2',  Jlovements  of  the 
lower  facial  muscles ;  3,  Movements  of  the  tongue  and  jaws ;  4,  Jlovements  of  8ui)erior  extremity  ;  5, 
Jlovements  of  inferior  extremity ;  6,  Movements  of  the  ocular  muscles ;  7,  Movements  in  relation  with 
the  sense  of  hearing. 


next,  and  those  of  the  leg  last.  When  the  lesion  is  situated  wholly  in 
the  motor  area  consciousness  is  either  not  much  affected,  or  it  is  lost  at 
a  comparatively  late  period  of  the  spasm,  but  when  it  is  situated  in  the 
prefrontal  area  of  the  cortex,  consciousness  is  lost  Ijefore  the  commence- 
ment of  the  spasm  or  soon  after  it  begins.  And  when  the  lesion  is 
situated  in  the  occipital  or  temporo-sphenoidal  lobes,  the  spasm  is  pre- 
ceded by  some  disturbance  of  sight  or  of  hearing  respectively. 

In  idiopathic  epilep.sy  no  constant  anatomical  changes  have  been 
found  in  the  nervous  system,  but  such  changes  as  have  been  discovered, 
like  atrophy  of  one  of  the  hippocampi  majores,  have  generally  affected 


CEREBRO-SPINAL    SPASMS.  349 

the  cortex  of  the  brain.     The  lesion  of  idiopathic  epilepsy  is,  therefore, 
regarded  as  a  molecular  disturbance. 

Dr.  Todd  was  the  first  to  suggest  that  epilepsy  was  caused  by  an 
explosion  of  nerve  force,  but  this  theory  has  assumed  a  definite  shape 
in  the  hands  of  Dr.  Hughlings-Jackson,  who  advanced  the  opinion 
that  all  convulsions  which  are  attended  by  loss  of  consciousness  are 
caused  by  discharging  lesions  of  the  cortex  of  the  brain.  This  hy- 
pothesis has  received  a  considerable  amount  of  experimental  verifica- 
tion. Hitzig  Avas  able  to  determine  epileptic  paroxysms  by  various  in- 
juries to  the  cortex  of  the  brain,  and  Ferrier  obtained  a  similar  result 
by  passing  a  faradic  current  of  moderate  intensity  through  the  cortex, 
the  electrodes  being  widely  separated,  so  that  a  large  portion  of  the 
cortex  was  included  in  the  circuit.  According  to  this  theory,  the  con- 
vulsions are  caused  by  a  large  discharge  of  nervous  energy  from  the 
cortex  of  the  brain  along  centrifugal  nerve  paths,  and  the  loss  of  con- 
sciousness is  caused  by  the  temporary  exhaustion  which  succeeds  to  an 
excessive  nervous  discharge.  But  we  have  seen  that  the  paroxysm  of 
unilateral  epilepsy  is  alwaj^s  followed  by  a  temporary  paralysis  of  the 
convulsed  limbs,  and  it  may  be  asked  why  it  is  that  the  paroxysm  of 
general  convulsions  is  not  likewise  followed  by  a  temporary  paralysis? 
The  reply  is  that  it  is  so  followed.  After  an  epileptic  attack  there  is 
complete  muscular  relaxation,  but  as  the  patient  is  at  the  same  time  in 
an  unconscious  condition  the  degree  of  paralysis  which  is  present  cannot 
be  estimated,  and  even  after  consciousness  is  regained  general  muscular 
feebleness  often  remains  for  a  time,  Avhich  although  not  called  paralysis  is 
really  paralytic  in  nature.  The  unseemly  and  apparently  immoral  actions 
performed,  and  the  atrocious  crimes  often  committed  by  patients  after 
minor  attacks  of  epilepsy,  may  be  explained  on  the  supposition  that 
the  inhibitory  influence  of  the  highest  centres  is  temporarily  suspended, 
thus  permitting  the  centres  which  preside  over  automatic  actions  and 
animal  instincts  to  spring  into  greater  activity. 

Many  of  the  spasmodic  phenomena  of  hysteria  are  best  explained 
on  the  supposition  that  the  irritability  of  the  cortex  of  the  brain  is 
increased,  whilst  others  are  best  explained  by  supposing  that  the  irrita- 
bility of  the  cortex  diminishes.  Hysterical  attacks  are  caused  by  a  dif- 
fused discharge  of  energy  from  the  cortex  of  the  brain,  while  local 
spasms  are  sometimes  caused  by  a  local  discharge  from  one  of  the 
motor  centres,  and  at  other  times,  especially  Avhen  they  assume  the 
form  of  persistent  contracture,  by  paralysis  of  one  of  these  centres, 
removing  the  inhibitory  action  of  the  brain,  and  thus  permitting  the 
unrestrained  action  of  inferior  ganglia.  Very  little  beyond  conjecture 
is  known   with  regard  to  the  pathology  of  catalepsy,  trance,  ecstasy, 


350  SPASMODIC    DISORDERS, 

somnambulism,  and  hypnotism,  but  there  can  be  but  little  doubt  that 
these  curious  conditions  are  caused  by  a  molecular  disturbance  of  the 
cells  and  fibres  of  the  cortex  of  the  brain,  or  of  the  conducting  paths 
which  lead  from  the  surface  of  the  body  to  the  cortex.  Hysterical 
hemianesthesia,  for  example,  is  best  ex})lained  by  supposing  that  the 
conduction  of  the  centripetal  fibres  in  their  ascent  through  the  internal 
capsule  is  temporarily  arrested.  Suppose  that  a  complete  bilateral 
hemianesthesia  exists,  what  would  be  the  condition  of  the  patient? 
There  would  be  complete  loss  of  every  form  of  cutaneous  and  muscular 
sensibility  as  well  as  of  sensation  in  the  bones  and  joints,  there  would 
be  loss  of  taste  on  both  sides  of  the  tongue,  and  of  smell  in  both  nos- 
trils, and  instead  of  there  being  amblyopia  and  partial  deafness  on  one 
side  as  in  hemianaesthesia,  there  would  be  complete  blindness  and  deaf- 
ness on  both  sides,  inasmuch  as,  according  to  the  hypothesis,  the  sen- 
sory centres  in  both  hemispheres  either  have  ceased  to  act,  or  the 
impressions  made  upon  the  peripheral  sense  organs  fail  to  be  conducted 
to  them.  But  impressions  made  on  the  periphery  would,  however, 
reach  the  cortex  of  the  brain  through  the  optic  thalamus,  and  the 
subject  of  bilateral  hemiansesthesia,  although  effectually  cut  off  from 
the  external  world  so  far  as  the  anatomical  substratum  of  consciousness 
is  concerned,  would  perform  various  complicated  actions  in  response  to 
peripheral  impressions,  but  without  being  attended  by  consciousness. 
The  state  of  the  patient  would,  indeed,  be  very  similar  to  that  observed 
in  somnambulism,  the  mesmeric  state,  and  various  post-epileptic  and 
allied  conditions. 

Treatment. — The  first  aim  of  treatment  is  to  Avithdraw  the  excitin"- 
cause  of  the  spasm,  and  with  this  view  all  sources  of  direct  irritation 
such  as  tumors  in  the  vicinity  of  the  nerve,  of  reflex  irritation  such  as 
conjunctivitis  in  blepharospasm,  carious  teeth  in  facial  spasm,  and  irri- 
tating substances  in  the  atmosphere  in  sneezing,  and  of  remote  irritation 
such  as  uterine  disease  in  facial  spasm  or  spasmodic  torticollis,  must  be 
removed.  The  source  of  irritation  may  be  found  in  impure  blood,  and 
if  the  patient  be  rheumatic  salicylate  of  soda  or  iodide  of  potassium, 
and  if  scrofulous,  carbonate  of  iron  and  cod-liver  oil  should  be  admin- 
istered. When  the  local  spasm  is  a  mere  expression  of  a  more  general 
nervous  disease  such  as  hysteria  or  chorea,  the  treatment  appropriate 
for  the  central  disease  must  be  adopted.  The  most  likely  internal 
remedies  for  such  cases  are  arsenic,  bromide  of  zinc,  and  bromide  of 
potassium.  The  local  application  of  chloroform  and  ether  spray,  and 
the  subcutaneous  injection  of  morphia,  will  be  found  useful  in  many 
cases  to  allay  the  distress  caused  by  the  spasm.  The  best  local  treat- 
ment,  however,  is  afforded  by  the  application  of  the    constant  cur- 


CEREBRO-SPINAL    SPASMS.  351 

rent.  A  descending  current  of  moderate  intensity  may  be  passed 
along  tlie  affected  nerve,  and  when  points  of  arrest  are  obtained  the 
anode  shoukl  be  phaced  over  one  of  these.  The  antagonists  of  the 
affected  muscles  may  be  strengthened  by  the  use  of  the  ftiradic  current, 
but  the  interrujjted  current  should  never  be  applied  directly  to  muscles 
Avhich  are  the  subjects  of  spasm.  Some  cases  of  spasm  are  benefited 
by  the  application  of  a  strong  galvanic  current  over  the  vertebi'al  column, 
the  part  of  the  cord  from  which  the  affected  nerve  is  derived  beino-  in- 
cluded in  the  circuit.  Continuous  pressure  over  the  affected  nerve  bv 
means  of  a  compress  or  suitable  mechanical  appliance  at  a  point  at 
which  it  emerges  from  a  bony  canal  or  becomes  superficial  has  been 
found  useful  in  the  treatment  of  spasm.  In  some  cases  the  pressure  is 
more  successful  when  applied  over  one  of  the  "spasm-arresting  points'" 
of  the  fifth  nerve  in  fecial  spasm,  in  the  length  of  the  affected  muscles 
in  other  cases. 

Various  surgical  operations  have  been  resorted  to  for  the  cure  of  local 
spasms.  Subcutaneous  division  of  muscles  and  of  tendons  is  most  likely 
to  be  of  use  in  the  tonic  form  of  spasm.  Division  of  the  spinal  accessory 
nerve  has  been  successful  in  several  cases  of  spasmodic  torticollis,  but 
section  of  the  facial  nerve  causes  paralysis  of  such  a  large  number  of 
important  muscles  that  it  is  hardly  a  justifiable  operation.  Stretching 
of  the  nerve  has,  however,  been  attended  with  very  favorable  results  in 
several  cases.  In  spasms  of  groups  of  muscles  of  the  extremities  various 
mechanical  contrivances  may  be  employed  in  order  to  force  and  maintain 
the  limb  in  a  normal  position.  In  spasmodic  torticollis  the  head  may 
likewise  be  maintained  in  the  normal  position  by  means  of  a  Sayre's 
jacket  with  jury-mast.  Another  method  is  to  surround  the  head  and 
the  trunk  each  by  a  plaster-of-Paris  bandage,  and  to  connect  the  tAvo  by 
a  strong  India-rubber  band  passing  obliquely  from  one  side  to  the  other 
in  such  a  position  as  to  counteract  the  spasm  of  the  affected  muscle. 
Professional  cramps  must  be  treated  on  the  same  general  principles  as 
other  forms  of  local  spasm.  In  slight  and  recent  cases  rest  for  a  period 
of  from  two  to  three  months  will  alone  suffice  for  a  cure,  but  this  period 
must  be  prolonged  to  from  six  to  twelve  months  in  severe  cases. 

The  most  successful  treatment  of  writer's  cramp  appears  to  be  that 
practised  by  Wolff,  which  is  a  combination  of  gymnastics  and  massage. 
The  gymnastic  exercis.es  consist  of  both  active  and  passive  movements. 
In  the  active  form  of  exercise  the  patient  is  instructed  to  execute,  three 
or  four  times  a  day,  a  series  of  vigorous  movements  with  the  affected 
extremity,  the  hand  being  opened  and  closed  in  quick  succession.  The 
number  of  these  movements,  and  consequently  the  duration  of  each 
exercise,  is   progressively  increased  until  a   duration  of  about  half  an 


352  SPASMODIC    DISOKDERS. 

hour  is  attained  for  each  sitting.  In  the  passive  movements  the  operator 
makes  forcible  traction  three  or  four  times  a  day  upon  each  of  the 
affected  muscles  separately  in  the  direction  of  its  length.  This  appears 
to  be  the  most  delicate  part  of  the  treatment,  inasmuch  as  if  too  little 
strength  is  employed  the  cure  is  delayed,  and  if  too  much  the  disorder 
is  aggravated.  When  the  spasm  is  notably  diminished,  which  usually 
occurs  in  a  short  time,  the  patient  is  encouraged  to  take  slow  and  grad- 
uated exercises  in  writing.  The  operator  practises  daily  massage  of  the 
affected  extremity,  particular  stress  being  laid  upon  percussion  over 
the  affected  muscles  with  the  ulnar  border  of  the  hand.  When  no 
amelioration  of  the  symptoms  is  produced  in  four  or  five  sittings,  Wolff 
believes  that  the  treatment  maybe  abandoned  as  not  likely  to  prove 
useful.  The  treatment  by  massage  is  applicable  to  spasms  of  other 
muscles,  and  several  cases  of  spasmodic  torticollis  in  which  I  prescribed 
it,  were  much  benefited. 

3Iechaniecd  means  have  been  resorted  to  in  severe  cases.  The  simplest 
method  of  this  kind  is  to  insert  the  pen  into  a  cork  or  thick  piece  of 
wood,  or  to  fasten  it  by  means  of  a  ring  to  the  first  or  middle  finger. 
Many  patients  are  relieved  by  applying  a  narrow  bandage  or  a  strip  of 
court-plaster  firmly-round  the  wrist. 

Tenotomy  of  the  affected  muscles  has  been  performed,  but  the  results 
obtained  have  not  been  very  encouraging.  The  treatment  of  other 
professional  spasms  must  be  conducted  on  essentially  similar  principles. 
Very  little  is  known  with  regard  to  the  treatment  of  saltatory  spasm, 
but  the  agents  most  worthy  of  trial  are  morphine,  bromide  of  potassium, 
calabar  bean,  ergotine.  conium,  and  atropine. 

In  tetanus  the  great  aim  of  treatment  is  to  diminish  the  irritability 
of  the  gray  matter  of  the  spinal  cord.  The  agents  which  have  been 
used  for  this  purpose  are  chloral  hydrate,  bromide  of  potassium,  calabar 
bean  or  cannabis  indica,  nicotine,  chloroform,  and  morphine.  The  cold 
bath  and  cold  douche  may  be  used  Avhen  there  is  a  sudden  elevation  of 
temperature,  and  under  these  circumstances  the  patient  may  be  placed 
in  a  bath  of  about  90°  F.,  and  the  temperature  should  be  gradually 
reduced  to  60°  F.  by  the  addition  of  cold  water.  In  ordinary  cases  a 
warm  Ijath  is  soothing  to  the  patient.  The  patient  should  be  protected 
from  every  source  of  irritation,  such  as  noises,  strong  lights,  changes 
in  temperature,  and  sudden  contact.  His  strength  should  be  well 
supported,  and  when  he  is  unable  to  swallow  liquids,  owing  to  the 
spasm,  food  should  be  introduced  by  means  of  a  tube  passed  through 
the  nose  after  the  patient  has  been  brought  under  the  influence  of 
chloroform. 

In  tetany  the  causes  of  the  disease  must  be  carefully  inquired  into 


CEREBRO-SPIXAL    SPASMS.  353 

and  removed  when  possible.  The  diet  should  be  full  and  generous,  and 
Avhen  the  spasm  is  allayed  change  of  air  is  indicated.  Durino-  a  severe 
paroxysm  it  may  be  necessary  to  use  chloroform  inhalations,  opiates,  or 
belladonna,  and  bromide  of  potassium,  either  alone  or  in  combination 
with  chloral,  may  be  a  useful  adjunct  to  treatment.  The  galvanic  cur- 
rent to  the  contracted  muscles  has  often  proved  useflil. 

In  unilateral  convulsions  the  treatment  must  be  directed  against  the 
primary  disease,  and  the  possibility  of  syphilis  should  never  be  for- 
gotten. In  the  treatment  of  functional  spasmodic  affections  the  greatest 
care  must  be  taken  to  discover  and  remove  any  source  of  peripheral 
irritation,  and  in  hysteria  great  attention  must  be  paid  to  the  treatment 
of  ovarian  and  uterine  disorders. 

In  the  treatment  of  epilepsy,  it  has  been  found  that  la-omide  of 
potassium  is  the  most  useful  drug,  and  to  do  good  it  must  be  given  in 
doses  ranging  from  ten  to  forty  grains  three  times  daily.  Large 
doses  of  this  salt  are  apt  to  produce  an  eruption  of  acne,  Avhich 
soon  subsides  when  the  drug  is  discontinued,  and  it  may  possibly  be 
prevented  by  combining  arsenic  with  the  bromide.  The  bromide  of 
sodium  or  of  ammonium  may  be  used  instead  of  the  potassium  salt,  as 
being  less  depressing  in  its  effects.  Chloral  hydrate  is  sometimes  a 
useful  adjunct  to  the  bromide  of  potassium.  The  salts  of  zinc  have  also 
proved  useful  in  the  treatment  of  epilepsy,  and  they  appear  to  be  more 
eflBcient  with  patients  under  twenty  years  of  age  than  with  those  of 
maturer  years.  The  oxide  may  be  given  in  doses  of  from  two  to  five 
grains  three  times  daily,  or  the  sulphate  may  be  administered  at  first 
in  doses  of  three  grains,  and  progressively  increased  to  scruple  doses 
three  times  daily.  The  bromide  of  zinc  has  been  given  in  gradually 
increasing  doses  until  a  scruple  is  taken  three  times  a  day.  The  oxide 
of  zinc  may  be  combined  with  extract  of  belladonna  or  hyoscyamus, 
or  with  the  powdered  root  of  valerian.  Iklladonna,  or  atropine  and 
digitalis  have  been  found  useful  in  the  treatment  of  epilepsy,  either 
alone  or  in  combination  with  one  of  the  bromide  salts. 

The  treatment  of  eclampsia  must  vary  according  to  the  cause  of  the 
convulsion,  but  during  the  attack  the  inhalation  of  chloroform  is  the 
most  generally  useful  method  of  treatment  for  arresting  the  spasm. 

The  general  treatment  of  hysteria  is  too  wide  a  subject  to  be  dis- 
cussed fully  in  this  place.  Bromide  of  potassium  is  found  very  useful 
in  the  treatment  of  hysterical  spasms,  but  the  administration  of  iron 
and  other  tonics,  with  attention  to  the  health  of  the  patient,  is  much 
more  generally  useful  than  any  special  remedies.  The  most  important 
part  of  the  treatment,  however,  consists  of  the  moral  management  of 
tlie   patient,   and    hysterical   patients    are  treated  with   much   greater 

23 


;^5J:  SPASMODIC    DISORDERS. 

success  in  the  wards  of  a  hospital  than  in  their  own  homes.  In 
aggravated  cases,  therefore,  the  patient  shoukl  be  removed  from  her 
home  and  relations,  and  placed  for  a  period  of  some  months  either  in 
a  public  institution  or  under  the  care  of  complete  strangers.  Tlie 
method  of  seclusion  from  her  friends  was  first,  so  for  as  I  know,  strongly 
insisted  upon  by  Dr.  R.  Brudenel  Carter,  and  it  forms  a  principal  factor 
in  the  treatment  of  hysterical  neurasthenia,  which  has  been  elaborated 
by  Dr.  S.  Weir  Mitchell,  and  which  has  already  been  described.  "The 
attacks,"  says  Dr.  Carter,  ''Avill,  in  all  probability,  occur  during  a 
meal,  or  when  there  are  strangers  present,  or  at  some  most  inconvenient 
time  and  place,  and  it  may,  on  this  account,  be  necessary  to  have  the 
patient  removed  to  her  bedroom.  In  such  case  she  should  be  carried 
there  as  quickly  as  possible,  placed  upon  the  floor,  and  immediately 
left  quite  alone,  the  door  being  shut,  and  no  one  being  suffered  to  open 
it  on  any  pretext  whatever  until  the  patient  does  so  herself.  But  if 
the  room  in  which  the  attack  takes  place  can  be  spared  for  a  few  hours, 
it  should  be  closed  and  shut  up  in  the  same  manner,  and  in  either  case 
especial  care  must  be  taken  not  to  give  utterance  to  a  single  expression, 
either  of  sympathy  or  alarm.  After  the  lapse  of  a  longer  or  shorter 
time,  often  at  a  meal,  and  sometimes  not  until  the  next  morning,  she 
will  present  herself  as  usual,  and  will  perhaps  offer  some  apology  or 
express  some  regret  for  her  illness.  This  should  be  graciously  received, 
and  then  every  attempt  on  her  part  to  return  to  the  subject  must  be 
carefully  and  industriously  foiled,  no  inquiries  being  made  about  her 
health,  and  all  complaints  being  interrupted  by  the  introduction  of 
ordinary  conversational  topics."  Treatment  by  isolation  is  only  to  be  rec- 
ommended in  very  aggravated  cases,  and  after  other  measures  have  failed. 
In  ordinary  hysterical  attacks  the  patient  takes  care  not  to  injure  her- 
self, but  it  is  often  necessary  to  prevent  respiration  being  impeded  by 
clothing.  In  my  experience  it  is  often  desirable  to  prevent  a  hysterical 
woman  from  tossing  about  violently  in  all  directions.  The  best  method 
of  preventing  the  patient's  struggles  is  to  place  an  attendant  on  each 
side  of  her,  and  to  direct  each  to  grasp  one  wrist  with  one  hand,  and 
to  hold  the  shoulder  firmly  down  to  the  bed  or  floor  with  the  other,  and 
if  necessary  the  legs  must  be  held  down  by  a  third  attendant.  It  is 
remarkable  how  soon  a  hysterical  patient  ceases  to  struggle  when  she 
finds  that  she  is  held  as  in  a  vice.  So  long  as  the  patient  can  shake  herself 
free  from  her  attendants,  so  long  is  the  struggle  likely  to  be  maintained, 
but  when  once  she  feels  that  she  is  thoroughly  restrained,  and  that  her 
efforts  do  not  find  outward  expression,  she  generally  ceases  to  struggle. 
The  most  usual  remedy  for  arresting  the  attack  is  to  dash  cold  water 
on  the  face  and  neck,  and  the  plan  suggested  by  Dr.  Hare,  of  forcibly 


CEREBRO-SPINAL    SPASMS.  355 

holding  the  mouth  and  nose  of  the  patient  so  as  to  prevent  her  from 
breathing,  is  still  more  effectual.  An  emetic  of  sulphate  of  zinc  is  also 
very  successful  in  arresting  the  attack. 

Local  spasms  in  hysteria  are  best  removed  by  general  treatment  and 
moral  management,  although  local  treatment  and  special  remedies  are 
occasionally  found  useful.  The  most  useful  local  remedies  are  the  cold 
douche  and  faradic  current. 

In  the  treatment  of  catalepsy  and  allied  conditions  the  best  results 
have  been  obtained  by  the  use  of  iron  and  other  tonics,  ergot,  the  cold 
douche,  and  the  faradic  current.  In  protracted  cases  artificial  feeding 
by  the  stomach  pump  and  nutritious  enemata  must  be  employed. 


CHAPTER    Y. 

ATROPHIC  PARALYSES. 

It  has  already  been  shown  that  the  various  forms  of  paralysis  may  be 
divided  into  spino-peripheral  or  atrophic,  and  cerebro-spinal  or  spasmodic 
paralyses.  The  spino-peripheral  paralyses  with  which  we  have  to  do  at 
present  may  be  divided  into  (I.)  simple  neural  paralyses  caused  by  local 
disease  or  injury  of  individual  motor  or  mixed  nerves ;  (II.)  multiple 
neural  paralyses  caused  by  disease  affecting  many  of  the  peripheral 
nerve  branches  and  often  assuming  a  progressive  character;  (HI.) 
reflex  paralyses  caused  by  iiiitation  of  afferent  nerve  fibres ;  (IV.) 
spinal  atrophic  paralyses  caused  by  disease  of  the  ganglion  cells  of  the 
anterior  gray  horns  of  the  spinal  cord,  and  to  these  may  be  added  (Y.) 
certain  forms  of  myopathic  paralysis. 

I.  SIMPLE    NEUKAL   PARALYSES. 

1.  Paralysis  of  the  Oculo-motok  Nerves. 

The  oculo-motor  nerves  are  the  oculo-motorius,  trochlearis,  and 
abducens,  and  the  subjoined  diagram  (Fig.  98)  Avill  suffice  to  remind 
the  reader  of  their  course  and  distribution. 

a.  Disorders  of  the  Movements  of  the  Eyelids. 

(1)  The  lev(^^ palpehrce  superioris  is  but  seldom  affected  by  tonic 
spasm  as  an  isolated  affection,  and  hardly  ever  by  clonic  spasm.  Tonic 
spasm  of  this  muscle  causes  the  lid  to  be  drawn  upwards,  and  there  is 
consequent  inability  to  close  the  eye,  either  by  voluntary  effort  or  during 
sleep.  The  orbicular  muscle  is  supplied  by  the  fiicial  nerve,  and  spasm 
of  it  will  be  subsequently  described. 

(2)  Paralysis  of  the  levator  palpebrce  superioris,  or  ptosis,  may  occur 
as  a  separate  affection,  but  it  is  usually  associated  Avith  paralysis  of  the 
superior  rectus,  both  muscles  being  supplied  l)y  the  superior  branch  of 
the  oculo-motor  nerve.  The  upper  lid  hangs  motionless,  the  palpebral 
aperture  is  greatly  narrowed,  the  lid  remains  motionless  when  the  eye  is 
directed  upwards,  and  the  horizontal  wrinkles  of  the  upper  lid  are 
effaced. 


SI.MPLE    XEURAL    PARALYSES.  ;— 


357 


(3)  Disorder  of  the  Associated  and  Mechanical  Movements  of  the 
Muscles  of  the  Eyelids. — When  the  eyes  are  directed  upwards  in  health 
there  is  an  associated  contraction  of  the  elevators  of  the  lids  and  the 
upper  eyelids  are  Tetracted,  and  when  the  eyes  are  directed  downwards 
there  is  a  simultaneous  downward  movement  of  the  upper  eyelids,  and 


Fig   98. 


DiAORAM   OF   THE   FiRST   OR   OPHTHAI.MIC   DiVISIiiX    OF   THE    FiFTlI,  SHOWING   ALSO   THE   TuiRD,   KlIURTH, 

AND  Sixth  Cranial  Xerves.     (From  Hermann's  "Phj'siology."') 

V,  Sensory  root  of  fifth  nerve. 

GG,  Gasserian  ganglion  on  larger  ruot  of  the  fifth  nerve. 

a,  Ophthalmic  division  of  the  fifth  nerve. 

1,  Frontal  nerve.     2,  Lachrymal  nerve.     3,  Xasal  nerve. 
LG,  Lachrj'mal  gland. 

.3',  Infra-trochlear  branch  of  nasal  nerce. 

3",  Long  ciliary  branches  of  nasal  nerve. 

3'",  Branch  of  nasal  nerve  to  ophthalmic  ganglion. 
OG,  Ophthalmic  ganglion. 

6,  Second  division  of  the  fiftli  cut  across,    c,  Third  division  of  fifth  cut  across. 

III,  Third  nerve  (motorius  oculi). 

4,  Upper  division  of  third  nerve.    5,  Lower  division  of  third  nerve,  near  point  where  it  gives 
the  short  root  to  the  ophthalmic  ganglion. 

IV,  Fourth  nerve  (n.  trochlearis). 

7,  Its  fibres  passing  to  the  superior  oblique. 

VI,  Sixth  nerve  (n.  abducens). 

0,  Its  fibres  passing  to  external  recttis. 
CA,  Carotid  artery. 
E,  Vertical  section  through  anterior  part  of  eyeball  ;  conjunctiva  indicated  by  dotted  line. 


^^ 


to  a  less  extent  of  the  lower  lids  also.  The  downward  movement  of  the 
upper  eyelid  is  most  probably  caused  by  an  inhibitory  cerebral  influence 
being  sent  to  the  elevator  of  the  eyelid  and  superior  rectus  muscles 
simultaneously  with  the  impulse  to  contraction  sent  to  the  inferior 
rectus,  while  the  depression  of  the  lower  eyelid  is  probably  caused  by 
pressure  of  the  cornea  against  it.  It  has  been  shown  by  Dr.  Gowers 
that  these  movements  are  disordered  in   partial  paralysis  of  the  third 


358 


A'TEOPHIC    PAR- 


nerve.  In  a  case  of  the  kind  under  my  care  tne  i^atient  in  looking 
forwards  manifests  a  slight  external  squint  of  the  right  eye  (Fig.  99), 
while  the  palpebral  aperture  on  that  side  is  a  little  smaller  than  the  other 


Pig.  99. 


Fig.  100. 


one.  When  the  patient  looks  up  (Fig.  100)  the  left  or  healthy  eye  is 
rotated  upwards,  and  there  is  a  simultaneous  upward  movement  of  both 
eyelids  on  that  side,  but,  as  usual,  the  eye  has  gained  on  the  lower  lid, 


Fig.  101. 


so  that  a  considerable  portion  of  the  sclerotic  between  the  lower  margin 
of  the  cornea  and  the « edge  of  the  lid  is  uncovered.  The  right  eye, 
however,  has  scarcely  moved,  and  the  lids  have  also  remained  stationary. 


SIMPLE    NEURAL    PARALYSES.  359 

But  the  most  striking  deformity  occurs  wlien  the  patient  looks  down. 
The  left  upper  eyelid  moves  downwards  in  association  with  the  down- 
ward rotation  of  the  eyeball,  but  the  right  eyelid  and  eyeball  remain 
comparatively  stationary,  and  the  patient  presents  the  singular  appear- 
ance of  looking  Avith  the  left  eye  at  an  object  lying  at  her  feet,  while 
the  right  eye  seems  to  be  looking  at  an  object  almost  on  a  level  with 
the  eye  (Fig.  101).  This  disorder  in  the  movements  of  the  eyelids  of 
the  right  side  is  caused  neither  by  spasm  of  the  levator  nor  by  paralysis 
of  the  orbicular,  because  the  patient  can  close  that  eye  with  as  much 
readiness  and  firmness  as  the  left  one.  The  immobility  of  the  right 
eyelids  must,  therefore,  be  caused  mainly  by  an  arrest  of  the  associated 
contraction  and  relaxation  of  the  levator  palpebrpe,  which  respectively 
occurs  during  upward  and  downward  rotation  of  the  eyeball. 

h.  Paralysis  of  the  Exteryial  Muscles  of  the  Eyeball. 

General  Etiology. 

Paralysis  of  one  or  more  of  the  ocular  muscles  may  be  caused  by 
cold,  exposure  of  the  eye  to  strong  impressions  of  light,  excessive 
smoking,  alcoholic  excess,  blows  on  the  eye,  penetrating  wounds  of 
the  orbit,  fracture  of  the  skull,  and  compression  of  the  nerves  by 
tumors.  But  the  most  frequent  and  important  causes  are  syphilitic 
deposits  and  the  degeneration  wdiicli  is  the  anatomical  substratum  of 
locomotor  ataxia.  Ocular  paralysis  is  also  caused  by  diphtheria,  and 
may  occasionally  be  a  sequel  of  other  acute  diseases. 

General  Symptoms. 

Diplopia. — If,  when  the  visual  axis  of  one  eye  is  directed  to  an 
object,  the  direction  of  the  other  deviates  from  it,  the  image  in  the  dis- 
torted eye  falls  on  an  eccentric  portion  of  the  retina,  and  two  objects 
instead  of  one  are  seen.  The  image  seen  on  the  healthy  eye  falls  on 
the  macula,  and  is  therefore  distinct,  but  the  image  seen  on  the  distorted 
eye  forms  upon  a  more  or  less  peripheric  region  of  the  retina,  and  is 
therefore  faint  and  more  or  less  confused ;  the  former  is  consequently 
called  the  true,  and  the  latter  the  false  image. 

Neutralization  of  the  False  Image. — When  the  paralysis  is  of  old 
date  the  patient  learns  to  perceive  objects  only  with  the  healthy  eye 
and  the  diplopia  disappears,  whilst  the  distorted  eye,  from  long-con- 
tinued disuse,  suffers  consecutive  amblyopia.  The  diplopia  may,  how- 
ever, be  made  to  reappear  by  placing  before  the  healthy  eye  a  colored 
glass,  which  differentiates  the  true  image  and  permits  that  of  the  dis- 
torted eye  to  be  perceived. 


360 


ATROPHIC    PARALYSES. 


Relation  of  the  Images  to  One  Another. — The  false  image  ahvays 
occupies,  with  reference  to  the  axis  of  vision,  an  opposite  position  to 
the  distortion  of  the  eye.  Assuming  the  left  eye  to  be  aftected,  the 
false  imaiT-e  is  displaced  horizontally  to  the  patient's  right  in  outward 
squint  (Fig.  102,  1),  horizontally  to  the  patient's  left  in  inward  squint 
(Fig.  102,  2);  the  false  is  above  the  true  in   downward  (Fig.  102, 

Fig.  102. 


In  the  above  diagram  the  thick  cross  represents  the  true  image,  tho  thin  cross  the/i(/«e  image.      The  left 
eye  is  supposed  to  be  affected  in  all  of  them.     (After  Bristow.) 

3  and  4),  and  below  it  in  upward  squint  (Fig.  102,  5  and  6).  In  out- 
ward or  inward  squint  the  images  are  vertical  and  parallel  Avith  one 
another,  but  in  all  other  forms  of  squint  the  oblique  muscles  rotate  the 
distorted  eyeball  and  the  false  becomes  tilted  with  reference  to  the  true 
image  (Fig.  102,  3,  4,  5,  and  6),  the  false  image  being  tilted  in  the 
opposite  direction  to  the  rotation  of  the  globe.  The  distance  between 
the  images  becomes  greater  as  the  object  is  moved  in  the  direction  of 
the  action  of  the  paralyzed  muscles. 

Vertigo. — Diplopia  causes  considerable  embarrassment  to  the  patient 
whilst  walking,  which  disappears  in  great  part  when  the  distorted  eye 


I 


SIMPLE    NEURAL    PAEALY.SES.  3H1 

is  closed.  In  ascending  a  stair,  for  instance,  he  sees  two  steps  for 
every  one,  and  not  knowing  upon  which  to  place  his  foot  becomes  con- 
fused and  stumbles.  Perception  of  distance  is  defective,  and  the  patient 
becomes  confused  on  endeavoring  to  grasp  objects.  This  constant  con- 
fusion causes  great  fatigue,  vertigo,  and  sometimes  vomiting. 

Compensating  Attitudes. — The  patient  instinctively  neutralizes  the 
perception  of  double  images  by  placing  the  head  in  such  an  attitude 
that  the  paralyzed  muscle  does  not  require  to  act,  and  then  the  visual 
axes  can  be  converged  upon  objects. 

Secondary  Deviation  of  thr  Sound  Eye. — This  condition  has  already 
been  described. 

False  Projection. — When  a  person  looks  at  an  object  Avith  one  eve 
only,  a  judgment  of  its  position  in  space  is  formed  by  the  sense  of 
effort  made  to  fix  the  object.  If  a  patient  with  paralysis  of  the  ex- 
ternal rectus  of  the  left  eye  be  asked  to  touch  an  object  coming  before 
him  from  the  left  or  paralyzed  side,  he  misses  it  by  carrying  his  finger 
too  far  to  the  left,  or  to  the  side  of  the  object  corresponding  to  that 
of  the  paralyzed  muscle.  The  difficulty  of  immediately  recognizing 
the  position  of  objects  in  space,  called  false  projection.,  is  caused  by 
the  fact  that  it  is  necessary  to  make  an  increased  effort  with  the  affected 
eye,  so  that  the  amount  of  rotation  is  overestimated,  and  consequently 
an  erroneous  judgment  of  the  position  of  the  body  in  space  is  formed. 

Secondary  contraction  of  the  antagonistic  muscles  often  occurs ;  it 
increases  the  extent  of  the  duration,  and  augments  the  distance  of  the 
double  images  from  one  another. 

Symptoms  of  Special  Forms  of  Paralysis. 

(1)  Complete  paralysis  of  the  oculo-motorius  gives  rise  to  paralytic 
exophthalmos,  ptosis,  divergent  strabismus,  dilatation  and  immobility 
of  the  pupil,  and  impairment  of  the  power  of  accommodation.  Every 
effort  to  move  the  eye  in  any  direction  causes  it  to  rotate  outwards 
and  downwards,  and  it  gradually  becomes  fixed  in  this  position  by  the 
secondary  contraction  of  the  external  rectus  and  superior  oblique. 
Double  images  appear  over  almost  the  Avhole  field  of  vision :  the  folse 
image  is  to  the  right  when  the  left  eye  is  affected,  the  two  images  are 
on  a  level  when  the  object  is  in  the  horizontal  position,  and  the  false 
appears  below-  the  true  image  when  the  object  is  below,  and  above  it 
when  the  object  is  above  the  horizontal  line.  Fixation  is  only  possible 
in  an  outward  and  downward  direction,  the  compensating  attitude  of 
the  head  is  a  very  oblique  position  backwards  and  towards  the  healthy 
side,  and  secondary  deviation  of  the  eye  takes  place  in  all  directions 
except  in  that  towards  the  affected  eye. 


362  ATROPHIC    PAEALYSES. 

(2)  Incomplete  Paralysis  of  the  Oculo-motorius. — {a)  Paralysis  of 
the  superior  rectus  gives  rise  to  strabismus  dorsum  vergens,  in  which 
the  affected  eye  is  rotated  dowiiAvards  and  a  little  outwards.  The 
false  is  seen  above  the  true  image  and  tilted  to  the  patient's  right 
when  the  left  eye  is  affected  (Fig.  102,  3) ;  the  vertical  distance  be- 
tween the  images  increases  according  as  the  eyes  are  directed  upwards 
and  outwards,  while  the  false  image  disappears  at  the  horizontal  line, 
provided  there  be  no  secondary  contraction  of  the  inferior  rectus. 
When  the  eyes  are  directed  downwards  objects  are  seen  single,  and  the 
head  is  thrown  back  in  order  to  counteract  the  paralysis. 

(6)  Paralysis  of  the  internal  rectus  gives  rise  to  strabismus  diver- 
gens,  and  the  eye  cannot  be  rotated  inwards  beyond  the  middle  line. 
The  images  are  vertical,  parallel,  and  on  the  same  plane;  the  lateral 
distance  between  them  increases  as  the  object  is  moved  towards  the 
sound  side,  and  the  false  image  is  to  the  patient's  right  when  the  left 
eye  is  affected  (Fig.  102, 1).  There  is  secondary  deviation  of  the  sound 
eye  outwards,  and  in  fixing  an  object  the  head  is  turned  towards  the 
healthy  side. 

ic)  Paralysis  of  the  inferior  rectus  gives  rise  to  strabismus  sursum 
veryens,  in  which  the  affected  eye  is  directed  upwards  and  slightly  out- 
wards. The  false  is  below  the  true  image  and  tilted  to  the  patient's 
left  when  the  left  eye  is  affected  (Fig.  102,  5).  The  false  image  dis- 
appears when  objects  are  held  above  the  horizontal  line,  but  double 
vision  reappears  whenever  the  line  of  vision  is  lowered,  and  conse- 
quently this  form  of  paralysis  is  very  troublesome  in  walking  and  in  all 
kinds  of  handiwork. 

(d)  Paralysis  of  the  inferior  oblique  gives  rise  to  a  squint  in  which 
the  eye  is  turned  slightly  down-svards  and  inwards.  The  false  image  is 
above  the  true  and  tilted  to  the  patient's  right  when  the  left  eye  is 
affected  (Fig.  102,  4).  Double  images  appear  when  the  eyes  are 
directed  upAvards  and  disappear  at  the  horizontal  line,  while  the  images 
become  more  and  more  separated,  l)oth  vertically  and  laterally,  and 
the  tilting  of  the  false  image  becomes  more  pronounced  according  as 
the  object  is  carried  upwards  and  outwards.  In  the  compensatory 
attitude  the  head  is  thrown  backwards  and  the  chin  turned  a  little 
towards  the  healthy  side. 

(3)  Paralysis  of  the  trochlear  nerve  gives  rise  to  a  moderate  squint  in 
which  the  eye  is  slightly  rotated  upwards  and  inwards.  Double  images 
appear  when  the  eyes  are  directed  dowuAvards,  and  become  more  and 
more  separated  both  vertically  and  laterally  according  as  the  olyect  is 
carried  downwards  and  outwards.  The  images  are  vertically  superim- 
posed, the  flilse  being  the  lower  and  the  more  remote  of  the  two,  and 


SIMPLE    NEUEAL    PARALYSES.  363 

Tilted  to  the  patient's  right  when  the  left  eye  is  affected  (Fig.  102,  6). 
The  secondary  deviation  is  usually  straight  downwards.  There  is  false 
projection  of  the  field  of  vision  downwards  and  a  little  outwards,  and 
the  head  is  inclined  forwards  and  turned  towards  the  healthy  side.  The 
feeling  of  giddiness  is  often  well  marked. 

(4)  Paralysis  of  the  abdueens  nerve  gives  rise  to  strabismus  ron- 
vergens,  and  the  eye  cannot  be  rotated  outwards  beyond  the  middle 
line.  Double  images  are  seen  when  the  eyes  are  turned  horizontally  to 
the  paralyzed  side,  the  distance  between  them  increases  according  as 
the  object  is  moved  to  that  side ;  the  images  are  vertical  and  parallel, 
and  the  false  one  is  to  the  left  of  the  patient  when  the  left  eye  is 
affected  (Fig.  102,  2).  Secondary  deviation  occurs  to  the  inner  side, 
there  is  false  projection  of  the  field  of  vision  towards  the  outer  side, 
and  the  head  is  turned  towards  the  affected  side.  The  feeling  of  o-iddi- 
ness  is  severe,  and  may  be  accompanied  by  nausea  and  vomiting. 

(5)  Paralysis  of  the  ciliary  muscle,  (cycloplegia)  renders  the  patient, 
if  not  myopic,  unable  to  focus  small  objects  or- read  small  print,  and  he 
forms  an  incorrect  estimate  of  the  size  and'  distance  of  small  objects. 
It  is  often  complicated  by  mydriasis,  although  it  may  occur  as  an  inde- 
pendent affection. 

2.  Masticatory  Paralysis. 

Etiology. — Paralysis  of  the  trigeminus  is  rare  as  a  result  of  lesions 
of  the  nerve  in  its  extracranial  course,  but  generally  results  from  intra- 
cranial lesions  such  as  periostitis,  exostoses,  caries,  extravasations,  and 
tumors,  which  compress  the  nerve  at  the  base  of  the  skull.  It  is  also 
caused  by  lesions  of  the  pons  and  occasionally  by  lesions  of  the  cortex 
of  the  brain. 

Symptoms. — "When  the  paralysis  is  unilateral  there  is  difficulty  or 
impossibility  of  masticating  food  on  that  side,  and  the  lateral  move- 
ments towards  the  sound  side  are  rendered  impossible  by  paralysis  of 
the  pterygoids.  The  affected  muscles  are  often  felt  to  be  wasted,  and 
they  remain  flaccid  during  mastication,  while  those  of  the  opposite  side 
feel  rigid  at  each  contraction.  The  paralyzed  muscles  may  occasionally 
manifest  the  "reaction  of  degeneration."  The  tensor  veli  palati  is 
supplied  by  the  fifth  nerve,  but  paralysis  of  this  muscle  has  not  been 
observed  along  with  masticatory  paralysis.  The  tensor  tympani  is  also 
supplied  by  the  fifth  nerve,  and  it  is  probable  that  disorders  of  hearing 
may  accompany  masticatory  paralj'^sis  in  the  absence  of  any  lesion  of 
the  auditory  nerve,  consisting  of  noises  in  the  ears,  and  a  diminished 
power  of  appreciating  deep  tones.  The  paralyzed  muscles  may  become 
atrophied,  and  they  then,  as  a  rule,  manifest  the  reaction  of  degeneration. 


8(34  ATROPHIC    PARALYSES.  ^ 

When  the  aflfection  is  bilateral  the  patient  suffers  great  fatigue  during 
mastication,  and  he  is  forced  to  eat  only  fluid  and  pulpy  nourishment. 
When  the  paralysis  is  complete  the  lower  jaw  falls  down  with  its  own 
weight ;  at  other  times  the  jaw  is  fixed  by  secondary  contraction  of 
the  paralyzed  muscles.  Bilateral  masticatory  paralysis  is  generally  met 
with  as  a  part  of  labio-glosso-laryngeal  paralysis. 

Sensoty  disorders  usually  accompany  unilateral  masticatory  paralysis, 
and  the  sensory  branches  of  the  nerve  are  often  implicated  in  the  absence 
of  any  paralysis  of  the  motor  branch.  When  all  the  branches  of  the 
nerve  are  affected,  one  side  of  the  face,  part  of  the  ear,  the  skin  of  the 
temple  and  forepart  of  the  head,  conjunctiva,  cornea,  nasal  and  oral 
mucous  membranes,  tongue,  gums,  and  part  of  the  pliarynx  are  all 
rendered  more  or  less  completely  insensitive  on  the  affected  side, 
but  violent  eccentric  pains  may  be  felt  in  the  anaesthetic  area  (anics- 
thesia  dolorosa).  When  the  patient  puts  a  cup  to  his  lips  it  gives  him 
the  impression  of  being  broken,  as  he  can  only  feel  with  one-half  of 
the  lip. 

On  the  affected  side  the  skin  of  the  face  is  cold  and  often  of  a  bluish 
color  ;  the  gums  are  spongy ;  the  mucous  membrane  of  the  mouth  and 
nostril  may  ulcerate  and  bleed  ;  and  neuroparalytic  ophthalmia  is  apt 
to  occur.  Irritation  of  the  nasal  mucous  membrane  by  ammonia  or 
snuff,  on  the  affected  side  does  not  excite  sneezing,  and  the  sense  of  smell 
on  that  side  is  diminished  owing  partly  to  dryness  of  the  Schneiderian 
membrane  and  partly  to  the  nutritive  changes  which  take  place  in  it. 
The  sense  of  taste  in  the  anterior  two-thirds  of  the  anaesthetic  side  of 
the  tongue  is  lost  in  those  cases  only  in  which  the  lesion  is  situated  at 
the  base  of  the  skull,  or  in  the  lingual  branch  of  the  nerve.  When  the 
anaesthesia  is  of  peripheral  origin,  reflex  actions  are  abolished.  The 
extent  of  the  anaesthesia  will  of  course  vary  according  to  the  seat  of 
the  disease,  and  it  may  sometimes  be  limited  to  the  area  of  distribution 
of  a  single  branch  of  the  nerve. 

Diagnosis. — The  chief  difficulty  in  diagnosis  is  to  discover  the  locality 
of  the  primary  lesion,  and  for  the  determination  of  this  point  the  fol- 
lowing rules  modified  from  Romberg  may  be  of  use : 

(a)  The  more  the  anaesthesia  is  confined  to  slight  filaments  of  the 
nerve  the  more  peripheral  Avill  the  seat  of  the  lesion  be. 

(b)  If  the  loss  of  sensation  affect  a  portion  of  the  face  together  with 
the  corresponding  facial  cavity,  one  of  the  divisions  of  the  nerve  is 
affected  before  or  immediately  after  its  passage  through  the  cranium. 

(c)  When  the  entire  area  of  the  fifth  is  more  or  less  anaesthetic,  and 
there  are  nutritive  disorders  in  the  affected  pai-ts,  the  Gasserian  ganglion 
or  the  nerve  in  its  immediate  vicinity  is  the  seat  of  the  disease. 


.SIMPLE    NEURAL    PAEALYSES.  365 

(d)  If  the  antesthesia  of  the  fifth  nerve  is  complicated  with  disordered 
function  of  adjoining  nerves,  it  may  be  assumed  that  the  disease  is  seated 
at  the  base  of  the  brain. 

(f)  If  sensation  is  lost  in  the  face  on  one  side,  and  in  half  of  the 
body  and  limbs  on  the  other  side,  the  lesion  is  probably  situated  in  the 
lateral  part  of  the  upper  end  of  the  medulla. 

(f)  If  sensation  is  lost  in  the  face,  half  of  the  body,  and  the  limbs  on 
the  same  side,  the  lesion  is  situated  in  the  opposite  hemisphere  of  the 
brain,  most  })robably  in  or  near  the  posterior  third  of  the  posterior  seg- 
ment of  the  internal  capsule. 


3.  Paralysis  in  the  Area  of  Distribution  of  the  Seventh 
Nerve  (Mimetic  Paralysis,  Hemiplegia  and  Diplegia 
Facialis,  Prosopalgia,  Bell's  Paralysis). 

Paralysis  of  the  facial  nerve,  ■which  from  the  long  course  of  the  nerve 
and  its  exposed  position  is  frequently  observed,  may  be  (a)  unilateral  or 
(6)  bilateral.  The  branches  and  connections  of  the  nerve  are  shown  in 
Fig.  103. 

a.    Unilateral  Facial  Pai^alysis  [Honiplegia  Facialis). 

Etiology. — Exposure  of  one  side  of  the  face  to  cold  is  one  of  the 
most  frequent  causes  of  facial  paralysis,  it  is  then  called  rheumatic 
paralysis  although  most  probably  resulting  from  a  slight  neuritis.  Facial 
paralysis,  although  appearing  at  all  ages,  is  most  frequent  between 
twenty  and  forty  years  of  age,  and  sex  does  not  seem  to  exert  any 
influence  on  its  production,  and  each  side  of  the  face  is  about  equally 
liable  to  be  afiected.  It  frequently  results  from  injury  such  as  a  severe 
blow  on  the  ear,  gunshot  and  other  wounds,  and  fractures  of  the  temporal 
bone,  wdiile  in  association  with  paralysis  of  the  auditory  nerve  it  is  one 
of  the  most  common  signs  of  fracture  of  the  base  of  the  skull.  It  also 
occurs  after  extirpation  of  the  parotid  gland  and  other  surgical  opera- 
tions about  the  face  and  ear,  and  may  be  caused  in  newborn  infants  by 
pressure  of  the  forceps.  Disease  of  the  parotid  gland  or  of  neighboring 
parts  may  cause  facial  paralysis  either  by  pressure  on  the  nerve  or  by 
extension  of  the  morbid  process  to  it.  Various  diseases  of  the  ear  may 
cause  facial  paralysis,  and  of  all  the  causes  suppurative  otitis  interna, 
followed  by  destructive  changes  in  the  temporal  bone,  is  probably  the 
most  frequent.  Bony  tumors,  and  neoplastic  formations  of  all  kinds 
in  the  internal  ear  may  lead  to  compression  and  destruction  of  the  nerve. 
Primary  disease  of  the  facial  nerve  is  occasionally  observed  as  a  com- 
plication or  sequel  of  acute  febrile  diseases  such  as  diphtheria  or  variola, 


366  ATllOPHIC    PAKALYSES. 

but  is  much  more  frequent  as  a  secondary  result  of  these  affections  from 
disease  of  the  temporal  bone.  Syphilitic  periostitis,  meningitis,  and 
exostoses,  or  gummata  at  the  base  of  the  skull,  brain,  temporal  bone, 
or  in  the  sheath  of  the  nerve  itself,  may  produce  paralysis  by  com- 
pressing the  nerve.  Some  persons  appear  to  be  predisposed  to  facial 
paralysis.  Eulenburg  mentions  the  case  of  a  young  man  who  suffered 
twice  from  right-sided,  and  thrice  from  left-sided  facial  paralysis.  Facial 
paralysis  may  occur  as  a  rare  symptom  of  some  diseases  of  the  spinal 
cord  when  the  morbid  process  extends  upwards  to  the  medulla,  and  it 
may  occur  occasionally  in  tabes  dorsalis,  and  as  a  rare  complication  in 
tetanus. 

Symptoms. — Premonitory  symptoms  consisting  of  pain,  noises  in  the 
ear,  deafness,  and  abnormal  sensations  of  taste  on  the  side  which  is 
subsequently  attacked  with  paralysis  may  be  experienced  for  some  days 
before  the  loss  of  motor  power  declares  itself.  The  symptoms  of  com- 
plete unilateral  facial  paralysis  are  very  characteristic.  The  affected 
side  loses  its  wrinkles  and  furrows  and  appears  smooth,  flaccid,  and 
expressionless  ;  while  it  appears  puffy  and  falls  to  a  lower  level  than  the 
healthy  side.  The  patient  cannot  wrinkle  his  forehead  or  elevate  his 
eyebrow  on  the  paralyzed  side  ;  he  is  also  unable  to  close  his  eye  and 
on  attempting  to  do  so  the  eyeball  rolls  upwards  and  inwards  or  occa- 
sionally upwards  and  outwards.  The  power  of  winking  is  lost  and 
the  eye  remains  open  during  sleep  (lagophthalmos),  and  being  no  longer 
protected  from  the  contact  of  foreign  particles  it  often  becomes  irritated 
and  inflamed.  Owing  to  paralysis  of  Horner's  muscle,  the  tears  cannot 
enter  the  lachrymal  canal,  and,  therefore,  flow  over  the  cheek.  The 
nostril  on  the  paralyzed  side  flills  in  during  inspiration  instead  of  expand- 
ing as  it  does  in  health,  the  tip  of  the  nose  is  sometimes  drawn  to  the 
healthy  side,  and  the  naso-labial  fold  is  obliterated.  The  mouth  is 
drawn  obliquely  over  to  the  healthy  side,  and  the  distortion  becomes 
more  pronounced  during  all  mimetic  movements,  such  as  crying,  laugh- 
ing, and  speaking.  Paralysis  of  tlie  buccinator  causes  the  cheek  to  puft' 
out  in  speaking,  and  during  other  expiratory  actions  ;  the  pronunciation 
of  the  labial  consonants  is  impaired ;  attempts  at  blowing  or  whistling 
fail  because  the  air  escapes  through  the  paralyzed  fissure  of  the  lips ; 
the  saliva  dribbles  from  the  affected  side ;  and  food  is  apt  to  accumulate 
between  the  inner  surface  of  the  cheek  and  the  teeth.  The  external 
muscles  of  the  ear  are  also  paralyzed,  but  since  these  muscles  are  not 
usually  under  voluntary  control,  impairment  of  movement  in  them  is 
not  readily  detected.  Signs  of  paralysis  of  the  platysma,  the  posterior 
belly  of  the  digastric,  and  the  stylo-hyoid  muscles  can  sometimes  be 
<liscovered.     If  the  lesion  of  the  nerve  is  situated  above  the  geniculate 


SIMPLE    NEURAL    PARALYSES, 


367 


ganglion,  the  levator  palati  and  azygos  uvulfB  become  paralyzed,  but  the 
symptoms  of  this  condition  will  be  fully  described  -when  the  various 
forms  of  paralysis  of  the  soft  palate  are  under  consideration.  If  the 
nerve  is  diseased  above  the  point  where  the  branch   to  the  stapedius  is 


Diagram  of  the  Facial  Nerve,  its  connections  and  branches.  (From  Hermann's  "Physiology.""; 
F,  The  facial  nerve.  A,  Auditory  nerve. 

1,  The  geniculate  ganglion. 

gsp,  Great  superficial  petrosal  nerve  connecting  the  facial  ami  Meckel's  ganglion. 

sxp,  Small  superficial  petrosal  nerve  connecting  the  facial  with  the  Otic  ganglion  and  with  the 

tympanic  hranch  of  the  glosso-pharyngeal. 
exp,  External  supei-ficial  petrosal  connecting  the  tacial  with  the  plexus  un  the  middle  meningeal 
artery. 
"2,  Chorda  tympani,  joining  lingual  nerve. 

3,  Nerve  to  stapedius  muscle. 

4,  Communicating  branch  with  the  ganglion  of  the  root  of  the  vagus. 

5,  Posterior  auricular  nerve. 

6,  Branch  to  the  stylo-hyoid  and  digastric  muscles. 

TF,  Temporo-facial  division ) 

,',„  rt      ■      c    ■  ^  ^■  ■  ■         r  to  muscles  of  expression. 

CF,  Cervico-facial  division    J  ^ 

V,  Fifth  nerve.  oJ,  Auriculo-temporal  branch. 

id,  Inferior  dental  nerve.  I,  Lingual  nerve. 

MO,  Meckel's  ganglion. 

iiG,  Otic  ganglion. 

SG,  Submaxillary  ganglion. 

IM,  Internal  maxillary  artery. 

MM,  Middle  meningeal  artery. 

P,  Pneumogastric  nerve. 

GP,  Glosso-pharyngeal  nerve. 

I,  Its  tympanic  branch  (nerve  of  .Jacobson). 

given  oif  (Fig.  103)  that  muscle  becomes  paralyzed,  and  the  membrana 
tympani  is  rendered  unduly  tense  by  the  unantagonized  action  of  the 
tensor  tympani,  a  condition  which  causes    an  abnormal  acuteness  for 


3(58  ATROPHIC    PARALYSES. 

hearing  musical  tones,  especially  deep  notes,  and  which  is  often  accom- 
panied by  a  subjective  sound  of  high  pitch. 

The  auditory  and  facial  nerves  are  simultaneously  affected  when  the 
lesion  is  situated  at  the  base  of  the  brain,  in  the  meatus  auditorius 
internus,  or  in  the  middle  ear  and  the  adjoining  parts  of  the  temporal 
bone,  and  then  the  patient  is  completely  deaf  on  the  affected  side. 

If  the  lesion  is  situated  anywhere  between  the  geniculate  ganglion 
and  the  point  where  the  chorda  tympani  leaves  the  facial,  the  sense  of 
taste  in  the  lateral  half  of  the  anterior  two-thirds  of  the  tongue  is  lost, 
and  the  patient  often  complains  of  abnormal  dryness  of  that  side  of  the 
mouth. 

The  sense  of  smell  is  occasionally  diminished  on  the  aiffected  side 
partly  from  dryness  of  the  nostril  from  the  tears  not  getting  into  the 
lachrymal  sac,  and  partly  from  interference  with  the  access  of  air  to  the 
olfactory  chambers  from  paralysis  of  the  nasal  muscles. 

The  tongue  is  never  paralyzed  in  lesions  of  the  facial  nerve,  but  there 
is  an  apparent  deviation  or  protrusion  because  the  mouth  is  drawn  over 
to  the  healthy  side.  Sensory  disorder.^  are  usually  absent,  but  when  the 
peripheral  divisions  are  affected,  branches  of  the  fifth  are  often  impli- 
cated and  then  there  are  corresponding  disturbances  of  sensibility. 

The  reflex  movements  are  lost  in  peripheral  paralysis  of  the  facial. 
There  are  no  manifest  secretory  disorders  of  the  face,  but  it  has  been 
found  that  subcutaneous  injection  of  pilocarpine  does  not  cause  sweating 
of  the  paralyzed  side  in  cases  of  peripheral  lesions  of  the  nerve.  The 
electrical  reactions  of  the  paralyzed  nerve  and  muscles  remain  normal 
in  slight  and  transitory  cases,  but  in  all  aggravated  forms  they  manifest 
the  "  reaction  of  degeneration." 

Spontaneous  movements  may  occur  in  the  muscles  during  recovery, 
and  at  times  the  twitching  may  be  so  marked  that  the  disease  looks  like 
facial  tic.  At  other  times  associated  movements  occur  in  the  paralyzed 
muscles.  "When,  for  instance,  an  attempt  is  made  to  close  the  eye,  the 
angle  of  the  mouth  is  drawn  outwards  and  upwards,  and  conversely, 
when  an  attempt  is  made  to  draw  the  angle  of  the  mouth  to  one  side, 
the  eyelids  contract ;  the  zygomatici  contract  when  an  attempt  is  made 
to  elevate  the  eyebrow.  The  paralyzed  eyelid  moves  or  falls  to  a  lower 
level  than  the  other  during  downward  rotation  of  the  eyeballs.  Reflex 
contraction  may  occur  in  the  paralyzed  muscles,  either  through  the  fifth 
nerve  by  touching  the  skin  or  eyelashes,  or  through  the  optic  nerves  by 
making  a  rapid  movement  towards  the  eyes. 


SIMPLE    NEURAL    PARALYSES.  369 

h.  Bilateral  Facial  Paralysis  {Diplegia  Facialis). 

Etiology. — BiLateral  facial  paralysis  often  results  from  simultaneous 
lesion  of  both  facial  nerves,  such  as  compression  of  them  by  a  tumor 
where  they  lie  close  together  at  the  base  of  the  skull  or  in  the  course  of  the 
fibres  through  the  medulla  oblongata  and  pons,  bilateral  otitis  interna,  or 
caries  of  both  temporal  bones.  It  is,  however,  more  fre(juentlv  observed 
in  connection  with  progressive  bulbar  paralysis,  and  it  may  occasionally 
result  from  lesions  in  the  cerebral  hemispheres,  but  these  cases  will  Ije 
subsequently  described. 

Syynptoms. — In  facial  diplegia  the  immobility  which  is  present  on  the 
one  side  in  the  unilateral  affection  now  appears  on  both  sides,  but  the 
oblique  position  of  the  mouth,  nose,  and  chin  is  absent.  The  face  is 
smooth,  fixed,  and  expressionless,  even  when  the  emotions  ai'e  powerfullv 
excited,  and  the  patient,  in  the  apt  language  of  Romberg,  "  lau<dis  and 
cries  as  from  behind  a  mask."  When  all  the  branches  of  both  nerves 
are  implicated  the  patient  is  unable  to  wink  or  close  either  eye,  and  the 
tears  flow  over  both  cheeks.  The  saliva  dribbles  when  the  head  is  bent 
forwards  ;  taste  is  abolished  in  the  anterior  two-thirds  of  the  tongue : 
and  the  mouth  may  be  abnormally  d]y  ;  paralysis  of  the  stapedii  muscles 
may  occasion  disorders  of  hearing,  and  paralysis  of  the  soft  palate  gives 
to  the  voice  a  nasal  quality  and  allows  fluid  to  escape  through  the  nose 
during  attempts  at  deglutition,  which  is  rendered  still  more  difficult  by 
paralysis  of  the  stylo-hyoid  and  digastric  muscles.  The  nostrils  fall  in 
during  inspiration,  a  condition  which  gives  rise  to  considerable  discomfort 
and  difficulty  in  breathing,  and  articulation  is  impaired,  as  is  manifested 
by  the  patient  being  unable  to  pronounce  the  vowels  o  and  u,  and  the 
labial  consonants. 

Diagnosis. — The  discrimination  of  facial  paralysis  from  other  dis- 
eases presents  no  difficulty  except  in  the  slighter  forms  of  the  affection, 
and  the  want  of  symmetry  between  the  two  sides  may  be  detected  by 
paying  careful  attention  to  the  play  of  the  features  under  varying 
emotions,  or  by  getting  the  patient  to  execute  complicated  movements, 
such  as  whistling,  showing  the  teeth,  and  pronouncing  difficult  words. 
The  principal  signs  by  which  the  disease  is  recognized  in  infants  are 
distortion  of  the  face  or  crying,  difficulty  of  sucking,  and  lagophthal- 
mos  during  sleep.  The  most  difficult  part  of  the  diagnosis  is  to  de- 
termine the  exact  position  of  the  lesion.  We  must,  in  the  first  i)lace, 
decide  Avhether  the  lesion  is  situated  in  the  fibres  which  connect  the 
facial  nuclei  in  the  pons  with  the  muscles — peripheral  paralysis,  or  in 


370  SPASMODIC    DISORDERS. 

the  fibres  Avhich  connect  the  facial  cortical  centres  Avith  the  nuclei  in  the 
pons — central  or  cerebral  facial  paralysis. 

Peripheral  facial  paralysis  is  characterized  by  the  presence  of  paral- 
ysis of  both  the  upper  and  lower  branches  of  the  nerve,  lagophthalmos 
durino-  sleep,  atrophy  with  the  reaction  of  degeneration  of  the  paralyzed 
muscles,  external  wounds  or  disease  in  the  vicinity  of  the  nerve,  and 
disease  of  other  nerves  which  lie  near  to  it  at  the  base  of  the  brain  or 
in  its  course,  while  there  is  an  alisence  of  hemiplegia  and  other  cerebral 
symptoms. 

Cerebral  facial  p)aralysis  is, characterized  by  the  presence  of  paralysis 
of  the  lower  branches  of  the  nerve  combined  with  hemiplegia  and  other 
cerebral  symptoms,  but  the  power  of  closing  the  eye  and  reflex  actions 
are  retained,  and  the  muscles  neither  undergo  atrophy  nor  manifest  the 
reaction  of  degeneration.  The  following  rules  will  enable  the  reader 
to  determine  the  exact  position  of  the  lesion  in  cases  of  peripheral 
paralysis  of  the  nerve: 

(1)  If  the  lesion  be  situated  external  to  the  Fallopian  canal,  the 
muscles  of  the  face  are  alone  paralyzed. 

(2)  If  the  lesion  be  situated  in  the  Fallopian  canal,  but  below  the 
point  at  which  the  chorda  tympani  leaves  the  facial,  the  muscles  of  tlie 
external  ear  are  paralyzed  in  addition  to  those  of  the  face. 

(3)  If  the  lesion  be  situated  between  the  point  at  which  tlie  chorda 
tympani  is  given  off  and  the  point  of  origin  of  the  small  branch  to 
the  stapedius,  there  are,  in  addition  to  the  symptoms  already  men- 
tioned, abolition  of  taste  on  the  lateral  half  of  the  anterior  two-thirds  of 
the  tongue,  and  diminution  of  the  salivary  secretion  on  the  affected 
side. 

(4)  If  the  lesion  be  situated  between  the  point  of  origin  of  the  nerve 
to  the  stapedius  and  the  geniculate  ganglion,  the  same  symptoms  are 
present,  along  Avith  abnormal  acuteness  of  hearing. 

(5)  If  the  geniculate  ganglion  itself  is  diseased  all  the  previous  signs 
are  present,  and  in  addition  paralysis  of  the  soft  palate  and  distortion  of 
the  uvula. 

(6)  If  the  lesion  be  situated  in  the  nerve  above  the  geniculate  gan- 
glion, all  the  previous  signs  are  present  except  the  disorder  of  the  sense 
of  taste,  but  the  auditory  nerve  is  frequently  implicated,  and  then  there 
is  dulness  of  hearing  on  the  affected  side. 

(7)  If  the  lesion  be  situated  in  the  pons  on  a  level  with  tlie  facial 
nerve,  paralysis  of  the  facial  muscles  is  accompanied  by  one  or  more  of 
the  following  symptoms,  namely:  Hemiplegia  of  the  opposite  side, 
paralysis  of  the  sixth,  auditory,  and  branches  of  the   fifth   nerves  on 


SIMPLE    NEURA].    PARALYSES.  371 

the  same  side,  and  a  staggering  gait  iitli  tendency  to  fall  towards  the 
side  affected  with  facial  paralysis. 

The  diagnosis  of  the  seat  of  the  lesion  in  cerebral  facial  paralysis  will 
be  subse(|uently  considered. 


4.  Paualysis  of  the  Muscles  Supplied  by  the  Hypoglossal 
Nerve  (Glossoplegia). 

Etiology. — Paralysis  of  half  of  the  tongue  occurs  in  hemiplegia, 
and  of  both  sides  in  the  various  forms  of  bulbar  paralysis.  Injury  of 
the  upper  part  of  the  vertebral  column,  such  as  fracture  of  the  atlas, 
may  implicate  the  hypoglossal  nerve,  and  unilateral  paralysis  with 
atrophy  of  the  tongue  may  occur  in  the  advanced  stages  of  tabes  dorsalis 
and  in  secondary  descending  sclerosis  when  the  ganglion  cells  of  the 
hypoglossal  nuclei  are  implicated.  The  nerve  may  be  injured  in  its 
peripheral  course  by  tumors  and  other  lesions  at  the  base  of  the  brain, 
or  by  extracranial  growths  and  wounds. 

Symptoms. — In  unilateral  paralysis  very  little  is  observed  when  the 
tongue  is  in  a  state  of  repose,  but  when  it  is  protruded  the  tip  is  seen 
to  deviate  to  the  paralyzed  side  in  consequence  of  the  predominance  of 
the  action  of  the  healthy  genioglossus,  which  directs  the  tip  of  the 
tongue  to  the  opposite  side.  The  various  movements  of  the  tongue 
can  only  be  imperfectly  or  not  at  all  performed  on  the  aifected  side. 

When  the  paralysis  is  bilateral  and  complete,  the  tongue  lies  immova- 
ble on  the  floor  of  the  cavity  of  the  mouth ;  it  is  relaxed,  often  atrophied, 
with  its  surface  wrinkled,  and  frequently  presenting  slight  fibrillary 
contractions  on  the  dorsum.  When  the  patient  lies  on  his  back  the 
paralyzed  tongue  falls  backwards  in  the  cavity  of  the  mouth,  and  by 
partially  closing  the  glottis  it  contributes  to  the  production  of  stertorous 
breathing  in  cases  of  apoplexy,  and  may  even  cause  asphyxia.  If 
the  paralysis  is  incomplete,  the  tongue  can  be  protruded,  but  the  patient 
is  unable  to  execute  complicated  movements,  such  as  raising  the  tip 
towards  the  roof  of  the  mouth,  directing  the  tip  towards  the  nose  after 
protrusion,  or  rolling  it  into  a  tubular  form.  In  bilateral  paralysis 
mastication  becomes  seriously  interfered  with,  because  the  food  can 
no  longer  be  rolled  about  in  the  mouth  and  placed  between  the  teeth, 
whilst  deglutition  is  impeded  because  the  bolus  cannot  be  properly 
collected  on  the  dorsum  of  the  tongue  and  pushed  backwards  into  the 
pharynx,  and  consequently  food  and  fluid  regurgitate  into  the  mouth, 
and  the  patient  is  annoyed  by  the  constant  accumulation  of  saliva. 
Articulation  becomes    indistinct,  difficulty  being  first    experienced  in 


572 


SPASMODIC    DISORDERS, 


singing  and  in  pronouncing  the  letters  s,  sh,  I,  e,  i,  and,  at  a  later 
period,  k,  g,  r,  etc.,  while  if  the  paralysis  be  bilateral,  complete,  and 
associated  with  atrophy,  vocal  speech  becomes  quite  inarticulate  and 
unintelligible,  this  condition  being  named  anartheca. 


Fig.  104. 


DiAGEAM   OF  THE   HYPOGLOSSAL   NeKVE,    ITS   CONXECriONS   AND    BRANCHES. 

H,  Hypoglossal  nerve.  p,  Pneumogastric  nerve. 

S,  Superior  cervical  gauglion  of  the  sympathetic.  L,  Lingual  nerve. 

IC,  lie,  IIIC,  The  three  upjier  cervical  nerves. 

1,  Communicating  branches  from  hypoglos-sal  to  ganglion  of  the  trunk  of  the  vagus. 

2,  Connecting  filaments  with  the  loop  of  first  and  second  cervical  nei  ves. 

3,  Branch  to  the  sympathetic. 

4,  Descendens  noni. 

5,  Branch  from  second  and  third  cervical  nerves  (conimunicantes  noni). 
fi,  Branch  to  thyro-hyoid. 

7,  Terminal  muscular  branches. 

8,  Communicating  branch  to  lingual  branch  of  the  fiftli. 


SIMPLE    NEURAL    PARALYSES.  373 

Dicupiosis  and  Prognosis. — The  best  method  of  testing  the  condition 
(if  tlie  lingual  muscles,  according  to  Hutchinson,  is  to  take  each  side  of 
the  tongue  between  the  finger  and  thumb  of  each  hand,  and  then  to 
re(|uest  the  patient  to  put  his  tongue  out.  If  half  is  paralyzed, 
that  side  remains  soft  and  flaccid,  while  the  healthy  side  becomes  firm 
and  stiff".  Paralysis  of  the  tongue  is,  however,  readily  detected  by 
asking  the  patient  to  protrude  it  or  to  perform  complicated  movements 
with  it,  such  as  turning  the  tip  towards  the  nose  after  protrusion,  and 
rolling  it  into  a  tube. 

The  situation  of  the  primary  lesion  must  be  determined  from  the 
concomitant  symptoms.  Unilateral  paralysis  of  the  organ  associated 
Avith  hemiplegia  is  caused  by  a  cerebral  lesion,  while  bilateral  paralysis 
in  association  with  paralysis  of  the  lips  and  soft  palate  is  caused  by  a 
l)ulbar  lesion.     The  prognosis  will  depend  upon  primary  lesion. 

5.  Paralysis  of  the  Pneumogastric  Nerve. 

The  distribution  of  the  pneumogastric  nerve  is  represented  in 
Fig.  105. 

a.  Paralysis  of  the  Soft  Palate. 

The  soft  palate  is  supplied  by  branches  from  the  pharyngeal  plexus, 
which  is  composed  not  only  of  branches  from  the  vagus,  but  also  of 
the  seventh,  the  glosso-pharyngeal,  and  the  sympathetic  nerves.  The 
levator  palati  and  the  azygos  uvul?e  are  supplied  from  the  seventh 
nerve,  but  the  part  Avhich  the  branches  of  the  other  nerves  take  in  the 
innervation  of  the  palate  has  not  yet  been  determined,  and  it  will, 
therefore,  be  more  convenient  to  group  together  all  the  motor  and  sen- 
sory disorders  to  which  the  palate  is  liable. 

Etiology. — Paralysis  of  the  soft  palate  occurs  in  connection  with 
Ijulbar  paralysis,  and  in  the  course  of  many  diseases  of  the  spinal  cord, 
Avhile  partial  paralysis  of  it  occurs  in  certain  cases  of  peripheral  lesions 
of  the  seventh  nerve. 

Sy7nptoins. — The  symptoms  differ  according  as  the  paralysis  is  partial 
or  complete. 

(1)  Paralysis  of  the  levator  palati  causes  the  velum  on  the  affected 
side  to  hang  loosely  downwards,  and  to  occupy  a  lower  position  during 
rest  than  the  sound  side.  Tickling  does  not  cause  the  uvula  to  be 
arched  upwards,  but  it  is  rendered  tense  transversely  by  the  action 
of  the  tensor  palati,  while  its  posterior  edge  is  drawn  slightly  down- 
wards by  the  action  of  the  palati  pharyngeus. 


374 


SPASMODIC    DISORDERS, 
Fig.  105. 


Diagram  of  the  Pneumogastric  and  Spinal 
Accessory  Nerves,  their  connections  and 
BRANCHES.     (From  Hermann's  "Physiology."') 

P,  Pneumogastric  neire. 
SA,  Spinal  accessory  ner\e. 
H,  Hypoglossal  nerve. 
GP,  Glosso-pbarjiigeal  nerve 
r,  Facial  nerve. 

S,  Superior  cervical  ganglion  of  the  sympatlietic. 
yr,  Ganglion  of  the  root  of  the  vagus. 
i/t,  Gdvglion  of  the  tniii];  of  the  vagus. 
1,  Auricular  branch  of  the  vagus   (Arnold's 

nerve). 
'Z,  Pharyngeal  branch. 

3,  (,'onvergence  of  nerves  to  form  phanjngtul 
plexus. 

4,  Superior  laryngeal  nerve. 
4',  Internal  bi-auch    of   superior   laryngral 

nerve 
4",  External  branch  Vf  superior  laryngeal 
nerve. 

5,  Inferior  laryugeal  nerve  (recurrent). 
5',   Cardiac    branch    of    inferior''  laryngeal 

nen-e. 
6  fi  G,  Cardiac  branches  of  the  vagus. 
7,  Convergence  of  branches  of  vagus  to   form 

cardiac  plexuses. 
.*<,  Pulmonarj'  branches. 
9,  (Esophageal  branches. 

10,  Gastric  branches. 

11,  Splenic  branches. 

12,  Hepatic  branches. 
SA,  Spinal  accessory  nerve. 

id,  Internal  division  of  spinal  accessory. 
ed,  External  division  of  spinal  accessory. 
IC,  IK",  IIIC,  IXC,  Cervical  nerves. 


SIMPLE    NEURAL    PARALYSES, 


375 


I 


(2)  Combined  paralysis  of  the  levator  palati  and  azygos  wnsch- 
occurs  in  lesions  of  the  seventh  nerve  situated  in  or  above  the  (genicu- 
late ganglion.  In  addition  to  the  symptoms  of  paralysis  of  the  levator 
the  uvula  is  distorted,  being  arched  obliquely  forwards  and  usually 
towards  the  healthy  side.  In  many  cases,  however,  the  tip  of  the 
uvula  is  directed  not  to  the  healthy  but  to  the  paralyzed  side,  the  con- 
vexity of  the  arch  Ijeing  then  turned  to  the  healthy  side  (Fig.  1(J6). 

Fig.  lOi;. 


'*«/j)W»W*i""'^^ 


Distortion  of  the  L'vila  ix  a  case  of  peripheral  paralysis  of  the  right  sihe  of  the  face. 

{After  Sanders.) 


Sanders  thought  that  the  last  form  of  distortion  was  caused  by  the 
action  of  the  palato-pharyngeus  exerting  a  greater  effect  on  the  uvula 
on  the  affected  side  than  it  can  exert  on  the  sound  side,  Init  this  ex- 
planation is  not  very  satisfactory. 

(3)  Combined  paralysis  of  the  levator  and  tennor  j^^^lttti  causes  the 
velum  to  hang  doAvn  deeper  than  when  the  levator  is  alone  paralyzed, 
and  the  velum  is  likewise  displaced  laterally  owing  to  the  unopposed 
action  of  the  tensor  of  the  opposite  side,  while  there  is  no  contraction 
on  the  affected  side  on  reflex  irritation.  Speech  has  a  more  nasal  (puility 
and  fluids  regurgitate  more  freely  through  the  nose  than  when  the 
levator  is  alone  affected. 

(4)  Paralysis  of  the  palato-pharyngeus  is  recognized  by  the  altered 
appearance  of  the  isthmus  of  the  fauces,  the  posterior  pillars  of  these 
being  widely  separated  from  one  another,  and  immovable. 

(5)  Bilateral  paralysis  of  all  the  muscles  of  the  soft  palate  causes 
the  palate  to  hang  loose  and  flapping  from  tlie  roof  of  the  moutli,  and 
its  activity  is  not  called  forth  during  deep  inspiration,  or  during  the 


376  SPASMODIC    DISORDERS. 

movements  of  deglutition  and  phonation.  The  speech  has  a  strongly 
nasal  quality ;  while  fluids  are  ejected  through  the  nose.  Deglutition 
is  rendered  still  more  difficult  when  paralysis  of  the  soft  palate  is  asso- 
ciated, as  frequently  happens,  with  paralysis  of  constrictors  of  the 
pharynx. 

The  sensory  disorders  Avliich  accompany  paralysis  of  the  soft  palate 
consist  of  hypera^sthesia  or  amTesthesia,  and  various  par;\?sthesicV  of  the 
mucous  membrane  of  the  soft  palate  and  pharynx.  Increased  sensitive- 
ness of  these  parts  is  often  met  with  in  nervous  and  hysterical  subjects, 
while  anesthesia  is  always  pi-esent  in  diphtheritic  and  progressive 
bulbar  paralysis,  and  is  frec^uently  met  with  in  the  insane.  Par<^s- 
thesi»  of  the  pharynx,  consisting  of  feelings  like  that  caused  by  the 
presence  in  the  throat  of  foreign  bodies,  such  as  a  fish-bone,  hair,  or 
some  hard  substance,  are  often  experienced  by  nervous  and  hysterical 
subjects. 

h.  Faralyns  of  the  Pharynx  {Dysphagia  Paralytica). 

Etiology. — Partial  paralysis  of  the  superior  constrictors  may  bo 
associated  with  paralvsis  of  the  soft  palate  after  diphtheria  and  syphilis, 
but  paralysis  of  all  the  muscles  of  the  pharynx  and  the  muscular  coat 
of  the  tx:sophagus  generally  results  from  compression  of  the  nerves  at 
the  base  of  the  skull  by  tumors,  local  diseases  of  the  pons  and  medulla, 
or  as  a  terminal  phenomenon  in  apoplexy. 

Symptoms. — When  the  muscles  of  the  pharynx  are  alone  paralyzed 
the  only  symptom  present  is  difficulty  in  deglutition  :  the  morsel  passes 
to  the  back  of  the  mouth,  but  remains  on  the  root  of  the  tongue  in  the 
glosso-epiglottidean  fossa,  or  even  over  the  epiglottis,  and  must,  on 
account  of  the  dyspnoea  to  which  it  gives  rise,  be  removed  by  means 
of  the  finger.  Fluids  run  along  the  dorsum  of  the  tongue,  and,  passing 
readily  into  the  larynx,  give  rise  to  attacks  of  suflbcative  cough  ;  whilst 
the  patient  instinctively  makes  strenuous  effi:>rts  to  pass  the  fluid  over  the 
epiglottis  by  throwing  the  head  backwards,  and  by  an  endeavor  to  bring 
the  root  of  the  tongue  as  near  as  possible  to  the  upper  end  of  the 
oesophagus.  Paralysis  of  the  superior  constrictor  allows  fluids  to  re- 
gurgitate through  the  nose  during  deglutition,  inasmuch  as  contraction 
of  this  muscle  is  necessary  to  complete  the  division  which  the  soft  palate 
forms  between  the  buccal  and  nasal  portions  of  the  pharynx  during 
swallowino;. 

c.  Paralysis' of  the  (Esophagus. 

In  isolated  paralysis  of  the  oesophagus  the  morsel  of  food  passes  from 
the  pharynx  into  the  oesophagus,  but  it  remains  fiist  in  the  cervical  por- 


SIMPLE    XEURAL    PARALYSES.  377 

tion  of  the  tube  or  regurgitates  into  the  mouth.  "When  it  remains  fast 
in  the  oesophagus  it  may  produce  compression  of  the  larynx  and  cause 
dyspnoea  and  the  other  symptoms  which  indicate  the  presence  of  a  foreign 
body.  In  paralysis  of  the  oesophagus  a  sound  can  be  passed  readily 
into  the  stomach. 


d.  Paralysis  of  the  Laryngeal  Branches  of  the  Vagus  {Aphonia 
Paralytiea,  Paralysis  of  the  Larynx). 

Etiology. — The  more  usual  causes  of  paralysis  of  the  larynx  are  gun- 
shot wounds  and  surgical  injuries  of  the  vagus  or  recurrent  laryngeal 
nerves,  or  compression  of  these  nerves  in  the  neck  or  mediastinum  by 
various  tumors,  such  as  enlarged  lymphatic  glands,  aneurism  of  the 
arch  of  the  aorta  or  of  the  carotid  and  subclavian  arteries,  and  cancer  of 
the  oesophagus,  trachea,  and  thyroid  gland.  Laryngeal  paralysis  results 
occasionally  from  bilateral  compression  of  the  spinal  accessory  nerves 
in  their  passage  through  the  foramen  lacerum  by  cancerous  infiltration 
at  the  base  of  the  skull.  It  may  also  be  caused  by  exposure  to  cold, 
and  excessive  speaking,  or  it  may  be  a  sequel  of  acute  diseases  like  diph- 
theria. As  a  symptom  of  central  disease  it  is  met  with  most  frequently 
in  hysteria,  but  it  sometimes  occurs  in  the  course  of  tabes  dorsalis, 
insular  sclerosis,  and  progressive  bulbar  paralysis.  Unilateral  paralysis 
of  the  vocal  cords  may  result  from  an  apoplectic  seizure  when  the  lesion 
is  situated  in  the  medulla  oblongata  and  more  rarely  from  injury  of  the 
cerebral  conducting  path  above  the  medulla. 

Symptoms. — If  paralysis  of  the  laryngeal  muscles  gives  rise  to  vocal 
and  respiratory  disorders  it  is  named  (1)  mixed  laryngeal  paralysis,  but 
if  disorders  of  respiration  are  alone  present  it  is  named  (2)  respiratory 
paralysis,  while  if  disorders  of  vocalization  are  alone  present  it  is  named 
(3)  phonetic  paralysis.  Paralysis  of  the  laryngeal  muscles  may  also 
be  divided  into  unilateral  and  bilateral,  complete  and  incomi)lete 
paralysis,  according  to  its  extent,  and  each  of  these  may  be  divided 
into  total  and  partial  paralysis,  according  to  its  degree.  Before  \)vo- 
ceeding  to  describe  the  symptoms  it  may  be  as  well  to  mention  the 
various  positions  assumed  by  the  glottis  under  different  circumstances. 
Passing  from  the  middle  line  outwards,  these  positions  are:  (1)  Com- 
plete closure  of  the  glottis  (Fig.  108,  LI,  LL),  produced  by  the  com- 
bined action  of  the  arytsenoidei  and  crico-arytnenoidei  muscles;  (2)  the 
cadaveric  position,  in  which  the  glottis  is  slightly  open,  as  it  is  found  in 
the  dead  body;  (3)  the  position  of  quiet  breathing,  in  which  the  glottis 


878 


SPASMODIC    DISOKDERS. 


is  more  open  than  in  tlie  last  position,  but  still  only  moderately  dilated 
(Fig.  107,  J,  I):  (4)  the  j^osition  of  deq)  inspiration,   in  which  the 

Fig.  107. 


Schema  of  a  Horizontal  Section  thkouoh  the  Lakvnx. 
/  /,  The  position  of  the  arytjenoid  cartilages  and  vocal  cords  during  cjuiet  breathing.    The  arrows 
indicate  the  direction  in  which  the  crico-arytsenoidei  postici  muscles  act.     //  //,  Position  of  the  arytenoid 
cartilages  in  consequence  of  contraction  of  these  muscles. 


Fui.    108. 


Schema  of  a  Horizontal  Section  through  the  Larynx,  showing  the  action  or  the  Aryt.enoid 

Muscles.    (From  Landois's  "Physiologie.'") 

1 1,  Position  of  the  arytenoid  cartilages  during  quiet  breathing.     The  arrows  show  the  direction  of  th.> 

action  of  the  muscles.     //  U,  Position  of  the  cartilages  when  the  muscles  are  contracted. 


SIMPLE    NEURAL    PARALYSES.  879 

glottis  is  widely  dilated  (Fig.  107,  //.  11):  (5)  the  position  in  wliicli 
the  glottis  vocalis  is  closed  and  the  glottis  respiratoria  open  (Fio- 
109,/,/).  ^    *■ 

Fig.  100. 


Schema  of  Horizontal  Section  through  the  Larynx,  illustrating  the  action  of  Crico-aryt.enoidei 

Laterales  Musci.es.     (From  Landois's  "  Physiologie  " ) 

II II,  Position  of  the  arytsenoid  cartilages  during  quiet  breathing.     The  arrows  show  the  direction  in 

which  the  muscles  act.     1 1,  Position  of  the  cartilages  when  the  muscles  are  contracted. 

(1)  Mixed  Laryngeal  Paralysis. 

Mixed  laryngeal  paralyses  are  caused  by  disease  of  the  recurrent 
laryngeal  nerves,  and  the  muscles  which  dilate  the  glottis  as  well  as 
those  which  render  tense  and  approximate  the  vocal  cords,  are  para- 
lyzed, giving  rise  to  disorders  of  vocalization  and  respiration.  The 
muscles  become  atrophied  as  in  other  forms  of  peripheral  paralysis, 
and  lose  their  faradic  contractility. 

(a)  In  complete  bilateral  paralysis  of  the  laryngeal  muscles  the 
glottis  assumes  the  cadaveric  position,  and  is  immovable  during  attempts 
at  phonation.  The  relaxed  cords  are  drawn  somewhat  downwards 
during  inspiration,  and  pushed  slightly  upwards,  and  probably  slightly 
removed  from  one  another  during  expiration,  but  these  slight  move- 
ments are  very  different  from  the  active  movements  caused  by  contract- 
ing muscles.  The  voice  is  weak  and  may  be  reduced  to  an  almost 
inaudible  whisper.  Respiration  is  not  much  interfered  with  when  the 
patient  is  at  rest,  but  dyspnoea  and  stridulous  inspiration  are  readily 
induced  on  slight  exertion  (Figs.  110-113). 

(h)  In  complete  unilateral  paralysis  of  the  laryngeal  muscles  the 
vocal  cord  of  the  corresponding  side  is  motionless,  its  free  edge  is 
slightly  removed  from  the  middle  line,  and  the  vocal  cord  of  the  sound 


380 


SPASMODIC    DISOKDERS, 


side  alone  vibrates  during  attempts  at  phonation.  The  voice  is  com- 
pletely lost,  but  more  frequently  it  is  harsh  and  discordant,  and  is 
liable"^to  break  into  falsetto  tones  on  the  slightest  strain. 

(c)  In  incomplete  paralysis,  whether  unilateral  or  bilateral,  the  power 
of  excursion  of  the  vocal  cord  is  merely  diminished  and  not  entirely 

lost. 

Fio.  110. 


LAKVXtiOscoi'ic  Ai'PEAiiAxi'Es  OF  THE  iNTEitiOR  OF  THE  i-ARYNx.     ( From  Landois's  "  rbysiologie." ) 
L.,  The  root  of  the  tongue;    V.  V.,  Glosso-epiglottidean  ligament;    E.,   The  epiglottis;    H.,  Glottis; 

L.  r.,  The  time  vocal  cord;   ,S.  M.,  Opening  into  the  sinus  of  Jlorgagni  ;  L.  v.  ».,  The  false  vocal  cords  ; 

S.  S.,  The  projection  of  the  cartilages  of  Santorini ;  P ,  Pharynx  wall  ;    11'.  »'.,  The  cartilages  of  Wrisbrrg 

in  the  ary-epiglottidean  ligament ;  N.  p.,  The  sinus  pyriformis. 


Fig.  111. 


Fig.  11 -J. 


Fig.  113. 


Flii.  lU. — LaUYXOOSCOPIC   appearance   of   the    LAltVXX    lU'RI.VG    VUIET    HRKATHINa. 
Fir,    112. — ThF,   LARYNGOSrOPIC    APPEARANCE   OF   THE    LARYNX    DURING   VOCALIZATION. 

Fic;.  113  — The  laryngo.«copic  appearance  of  the  larynx  dvring  deep  inspiration,  siiowini;  the 

BIFURCATION   OF   THE  TRACHEA. 


(2)  Kespiratory  Laryngeal  Paralysis. 

Respiratory  laryngeal  paralysis  occurs  when  the  muscles  which 
widen  the  aperture  of  the  glottis — the  crico-aryt?enoidei  postici — are 
paralyzed.  In  such  cases  the  voice  is  unaffected,  but  serious  disorders 
of  respiration  may  be  present.  Bilateral  compression  of  the  recurrent 
laryngeal  nerves  by  aneurism  or  other  tumor  causes  paralysis  of  the 
abductors  of  the  vocal  cords,  while  frequently  leaving  the  adductors 
unaffected. 


SIMPLE    XEUHAL    PARALYSES.  381 

{a)  111  coDiph'te  fiirali/sis  of  the  crico-aryt£enoi(lei  postici  the  vocal 
cords  assume  the  cadaveric  position,  just  as  in  complete  paralysis  of  all 
the  laryngeal  muscles.  But  in  isolated  paralysis  of  the  abductors  of 
the  larynx  the  approximation  and  parallelism  of  the  vocal  cords  can 
gtill  he  accomplished,  and  the  voice  is  unaffected,  but  the  glottis  does 
not  dilate  during  deep  inspiration,  and  the  cords  cannot  be  separated 
beyond  the  cadaveric  position.  The  respiratory  function  is  at  first 
only  slightly  interfered  with,  but  after  a  time  the  healthy  adductors 
undergo  "paralytic  contracture"  and  drag  the  vocal  cords  towards  the 
middle  line,  so  that  the  glottis  is  almost  completely  closed.  The  glottis 
is  then  converted  into  a  narrow  slit,  and  is  quite  inadequate  to  carry 
on  ordinary  respiration.  The  breathing  now  becomes  laborious  and  of 
the  "forced  costal  type,"  inspiration  is  prolonged  and  noisy,  as  in 
croup,  but  expiration  is  comparatively  easy  and  quick,  and  in  conse- 
quence of  the  difference  of  atmospheric  pressure  above  and  behnv  the 
constricted  part  the  larynx  moves  up  and  down  considerably  durin<T 
each  respiratory  act.  On  laryngoscopic  examination  it  is  seen  that  the 
vocal  cords  are  approximated  so  that  only  a.  narrow  linear  chink  is  left 
between  them,  and  during  forced  inspiration  the  cords  approach  each 
other  so  closely  as  almost  to  close  the  glottis  completely  instead  of 
separating  from  each  other  as  in  health.  The  cords  are  slightlv  sep- 
arated during  each  expiratory  act.  During  phonation  the  vocal  cords 
and  aryto?noid  cartilages  approach  each  other  in  a  perfectly  normal 
manner. 

[h)  Incomplete  7'espiratory  larynfieal  paralysis  may  exist  for  a  long 
time  without  giving  rise  to  difficulty  of  breathing  or  any  manifest 
symptoms,  but  the  condition  could  doubtless  be  detected  in  laryngo- 
scopic examination. 

(3)  Phoketic  Laryngeal  Paralysis. 

Plionetic  paralyses  occur  when  the  muscles  which  render  tense  and 
approximate  the  vocal  cords  are  paralyzed,  and  the  affection  of  voice 
may  vary  from  slight  hoarseness  to  complete  aphonia,  according  to  the 
degree  and  extent  of  paraljisis. 

\a)  In  bilateral  paralysis  of  the  adductors  the  glottis  is  partially  open, 
and  both  the  arytenoid  cartilages  and  the  vocal  cords  are  immovable 
during  attempts  at  phonation.  The  glottis  cannot  be  closed  in  cough- 
ing, on  making  an  effort,  or  during  deglutition,  while  there  is  complete 
aphonia. 

{h)  In  unilateral  paralysis  of  the  adductors  the  vocal  cord  of  the 
affected  side  is  removed   from   the  middle  line,  and  cannot  be  apju-oxi- 


382  SPASMODIC    DISOEDERS. 

mated  to  its  fellow.  Tlie  affected  vocal  cord  can  only  vibrate  with  its 
edge,  and  consequently  the  voice  is  feeble,  and  readily  assumes  the 
falsetto  character. 

{(')  In  incomplete  phonetic  laryngeal  paralysk  the  tensor  and  cou; 
strictor  muscles  of  the  vocal  cords  are  separately  paralyzed.  Aphonia 
is  a  symptom  of  paralysis  of  all  these  muscles,  but  it  is  most  marked 
in  those  cases  in  which  the  space  between  the  cartilages  remains  open, 
because  the  blast  of  air  escapes  through  the  patent  glottis  respiratoria. 
The  voice  may  not  be  much  affected  in  those  cases  in  which  the  carti- 
lages close  and  the  ligamentous  portion  remains  open,  because  the  blast 
of  air  must  pass  through  the  glottis  vocalis,  and  a  certain  degree  of 
vibration  of  the  cords  induced. 

(j)  In  paralysis  of  the  eric o-ihy void  muscles,  which  occurs  when 
the  superior  laryngeal  nerve  is  implicated,  either  directly  or  through 
the  spinal  accessory  nerve,  the  vocal  cords  cannot  be  rendered  tense, 
and  consequently  the  voice  becomes  hoarse  and  deep,  Avhile  the  produc- 
tion of  high  notes  is  difficult  or  impossible.  The  absence  of  tension  of 
the  crico-thyroid  muscles  during  vocalization  may  sometimes  be  per- 
ceived by  placing  the  finger  over  the  crico-thyroid  space.  Disease  of' 
the  superior  laryngeal  nerve  also  paralyzes  the  thyro-arytasno-epiglot- 
tidei,  and  the  epiglottis,  being  drawn  towards  the  tongue,  fails  to  be 
depressed  over  the  aperture  of  the  glottis  during  deglutition,  and  con- 
sequently food  and  drink  obtain  entrance  into  the  larynx.  Aniesthesia 
of  the  larynx  is  also  present,  and  consequently  the  reflex  act  of  cough- 
ing is  not  set  up  until  the  foreign  substance  has  passed  below  the  level 
of  the  vocal  cords,  and  thus  an  attack  of  pneumonia  is  likely  to  be 
provoked.  On  laryngoscopic  examination  the  glottis  is  seen  to  be  rep- 
resented by  a  wavy  line,  and  in  unilateral  paralysis  the  vocal  cord  on 
the  affected  side  remains  on  a  higher  level  than  its  fellow.  The  crlottis 
closes  completely  during  strong  expiratory  efforts  like  coughing,  and 
the  arytgenoid  cartilages  are  quite  movable  during  attempts  at  phonation. 

(jj)  Ii^  paralysis  of  the  thyro-arytcenoidel  the  ligamentous  part  of 
the  glottis  remains  open,  while  juxtaposition  of  the  arytsenoid  cartilages 
takes  place.  Rheumatic  laryngeal  paralysis  often  assumes  this  form, 
but  occasionally  all  the  muscles  may  be  affected. 

( jjj )  In  paralysis  of  the  crico-arytcenodei  laterales  the  glottis  remains 
open  in  the  form  of  a  tolerably  broad  ellipse. 

(iv)  In  paralysis  of  the  arytoenoidei  the  ligamentous  portion  closes 
almost  completely,  while  the  space  between  the  arytenoid  cartilages 
assumes  a  triangular  form.  This  is  the  kind  of  paralysis  which  gener- 
ally causes  hysterical  aplionia. 


SIMPLE    NEURAL    PARALYSES.  383 

The  senson/  disorders  which  occur  in  diseases  of  the  laryngeal 
nerves  consist,  in  addition  to  neuralgia,  of  hypergesthesia,  anesthesia, 
and  various  parsesthesise.  Hyperaesthesia  of  the  laryngeal  mucous 
membrane  gives  rise  to  excessive  reflex  actions  on  slight  provocation. 
Anaesthesia  of  the  larynx  occurs  in  diphtheritic  paralysis,  and  may  be, 
in  association  with  anaesthesia  of  the  pharynx,  one  of  the  earliest 
symptoms  of  bulbar  paralysis.  The  pari»sthesi;3e  consist  of  abnormal 
feelings  as  if  a  hair,  fish-bone,  or  morsel  of  food  had  lodged  in  the 
larynx,  while  a  laryngoscopic  examination  shows  the  absence  of  any 
foreign  body. 

{d)  Paralysis  of  the  trunk  of  the  vagus  aiid  of  the  //astrie  and 
cardiac  plexuses  has  already  been  considered. 


6.  Paralysis  of  the  Spinal  Accessory  Nerve. 

Etiology. — Paralysis  in  the  region  of  distribution  of  the  spinal  acces- 
sory nerve  is  generally  of  peripheral  origin,  and  is  caused  by  traumatic 
injuries  of  the  nerve  or  by  compression  by  tumors,  abscesses,  or  dis- 
eased bones  of  the  skull.  Paralysis  may  also  be  caused  by  exposure  to 
cold  or  by  neuritis  in  wliatever  way  produced,  and  it  may  likewise  arise 
as  a  part  of  progressive  muscular  atrophy.  Partial  paralysis  of  the 
nerve  may  be  caused  by  disease  of  the  four  or  five  upper  cervical 
vertebrae. 

Symptoms. — Paralysis  of  the  sterno-cleido-mastoid  or  trapezius  mus- 
cles may  be  unilateral  or  bilateral,  and  the  muscles  may  be  separately 
or  simultaneously  afiected. 

(1)  In  unilateral  j^aralysis  of  the  sterno-cleido-mastoid  the  head  is 
held  in  an  oblique  position,  the  chin  is  elevated  and  turned  towards 
the  affected  side,  the  prominence  of  the  healthy  muscle  on  its  move- 
ments being  resisted  is  absent,  and  the  head  can  only  be  moved  in  the 
direction  of  the  affected  muscle  with  difiiculty  and  by  the  aid  of  the 
other  muscles,  but  passive  movements  can  be  readily  jjerformed.  In 
chronic  cases  the  healthy  muscle  becomes  contracted,  and  the  head  is 
made  to  assume  a  permanently  oblique  position. 

(2)  In  bilateral  paralysis  of  the  sterno-cleido-mastoid  muscles  the 
head  is  held  straight,  but  rotation  of  it  can  only  be  performed  with 
difficulty,  especially  when  the  chin  is  elevated.  The  prominences  of 
the  muscles  are  absent,  the  neck  looks  wasted,  and  a  slight  depression 
is  produced  between  the  mastoid  process  and  the  sternum. 

(3)  In  unilateral  paralysis  of  the  trapezius  the  scapula  of  the  affected 
side  is  drawn  somewhat  downwards  and  forwards,  and  its  inner  border 


384 


SPASMODIC    DISORDEES. 
Fig.  114. 


\P 


Nerve.s  of  the  Cervkwl  Ple.xis. 
IC,  lie,  IIIC,  IVC,  First,  second,  third,  and  fourth  cervical  nerves. 

1,  Muscular  branch  to  rectus  capitus  posticus  major  and  minor. 
1',  Muscular  branch  to  obli(iuus  superior. 

1",  Muscular  branch  to  coniplexus. 

2,  Muscular  branch  to  oblii|Uus  inferior. 

2',  Muscular  branch  to  coniplexus  and  traclielo-mastoid. 
2",  JIuscular  branch  to  splenius. 

3,  Muscular  branch  to  muscles  of  the  neck. 

4,  Muscular  branch  to  muscles  of  the  neck. 

G  0,  Great  occipital  nerve,  cutaneous  to  posterior  part  of  scalji. 
CO,  Cutaneous  branch  to  posterior  part  of  scalp  and  back  of  neck. 

5,  Muscular  branches  to  rectus  capitis  lateralis. 

5',  jMuscular  branches  to  rectus  capitis  anticus  major  and  minor. 
■y",  Commuuicating  branches  with  hypoglossal  and  pneumogastric  nerves. 
SO,  Small  occipital  nerve 

Ti,  Musculur  branch  to  occipito-froutalis  mu.scle. 


SIMPLE    NEURAL    PARALYSES.  385 

is  separated  from  the  vertebral  column  and  assumes  an  oblique  position 
the  inferior  angle  being  nearer  than  the  superior  to  the  vertebral  column. 
The  acromion  process  falls  downwards  and  forwards,  the  projectino- 
clavicle  makes  the  supraclavicular  fossa  deeper  than  natural,  and  the 
posterior  and  superior  angle  of  the  scapula  can  be  felt  with  .unusual 
distinctness.  Paralysis  of  the  upper  portion  of  the  trapezius  alone 
renders  elevation  of  the  arm  above  the  horizontal  line  difficult. 

(4)  In  bilateral  paral^/ns  of  the  trapezius  the  symptoms  are  present 
on  both  sides,  both  shoulder-blades  fall  outwards  and  forwards,  the  head 
readily  sinks  on  the  chest,  and  some  difficulty  is  experienced  in  main- 
taining it  in  an  upright  position. 

(5)  In  combined  jjaralysis  of  the  sterno-eleido-)na8toid  aiid  trapezius 
muscles  the  symptoms  of  the  separate  paralyses  are  combined,  and  then 
the  laryngeal  muscles  are  not  infrequently  paralyzed. 

7.  Paralysis  of  the  Muscles  Supplied  by  the  Cervical  Plexus. 

(1)  Paralysis  of  the  Posterior  Muscles  of  the  Neck. 

Paralysis  of  the  posterior  muscles  of  the  neck  occurs  occasionally  in 
infantile  atrophic  paralysis  and  progressive  muscular  atrophy,  but  it  is 
not  easy  to  distinguish  separate  paralysis  of  the  individual  muscles. 
When  all  the  muscles  of  both  sides  of  the  back  of  the  neck  are  paralyzed 
the  head  can  no  longer  be  carried  erect,  but  the  patient  usually  carries 
it  inclined  backwards  and  supported  only  by  the  anterior  muscles  of  the 
neck.  When  the  head  is  moved  forwards  beyond  the  vertical  line  it  falls 
forwards  until  the  chin  rests  on  the  sternum,  and  the  patient  is  unable 
to  raise  it  in  opposition  to  the  slightest  resistance,  but  can  do  so  by  a 
peculiar  swinging  movement. 

(2)  Paredysis  of  the  Diaphragm. 

Etiology. — Paralysis  of  the  diaphragm  may  occur  as  a  late  symptom 
of  progressive  muscular  atrophy  ;  it  is  occasionally  observed  in  hysterical 
patients,  and  Duchenne  met  with  it  in  lead  poisoning.  It  may  also  be 
caused  by  exposure  to  cold,  compression  of  the  nerve  by  tumors,  and  in 
cervical  pachymeningitis  on  a  level  with  the  body  of  the  fourth  vertebra. 

Symptoms. — Diaphragmatic  paralysis  is  most  commonly  bilateral  aiid 
the  symptoms  are  then  highly  characteristic.  During  inspiration  the 
epigastrium  and  hypochondria  are  drawn  inwards  instead  of  being 
curved  outwards,  and  if  the  hand  be  placed  upon  the  epigastrium  the 
protrusion  caused  in  health  by  the  descending  diaphragm  during  inspira- 

25 


38(5 


ATROPHIC    PARALYSES. 
Fig.  115. 


Nerves  of  the  Brachial  Plexus.    (After  Flower.) 
VC,  VIC,  VIIC,  Vine,  ID,  IID,  HID,  Fifth,  sixth,  seventh,  and  eighth  cervical,  an  I  first,  sycund,  and 
third  dorsal  nerves. 
CB,  Communicating-  brancli  from  tlie  fourtli  cervical  nerve. 
P,  Phrenic  nerve. 


SIMPLE    NEURAL    PARALYSES.  387 


r,  c,  Dorsal  cutaneous  branches  from  the  tilth  cervical  to  the  thinl  ilor«al  nervi'. 
M,  Jl,  Branches  to  the  muscles  of  the  neck  and  back. 
B,  Branch  to  the  scalenus  medius. 
S',  Branch  to  the  subclavius  muscle. 

I,  I',  Branches  to  rhomboideus  major  and  rhomboideus  minor. 
SS,  Suprascapular  nerves : 

2,  Branch  to  supraspinatus  muscle. 

2',  Branch  to  infraspinatus  mtiscle. 

sj,  Branch  to  shoulder-joint. 
PT,  Posteiior  or  long  thoracic  (external  respiratory  of  Bell)  supplies  serratus  magnus. 
EAT,  External  anterior  thoracic  supplies  pectoralis  major. 
lAT,  Internal  anterior  thoracic  to  pectoralis  major  and  pectoralis  minor. 

II,  First  intercostal  nerve. 
21,  Second  intercostal  nerve. 

IH,  Intercosto-humeral  joins  nerve  of  Wrisberg. 

AC,  Anterior  cutaneous  nerves  of  the  thorax. 
31,  Third  intercostal  nerve. 

LC,  Lateral  cutaneous : 

a,  Anterior  branch. 
p,  Posterior  branch. 
OC,  Outer  cord  of  brachial  plexus. 
PC,  Posterior  cord  of  brachial  plexus. 
IC,  Inner  cord. 
MC,  Musculo-cutaneous  nerve. 

4,  Branches  to  coraco-brachialis. 

5,  Branches  to  biceps. 

5',  Branches  to  brachialis  anticus. 

6,  Anterior  cutaneous  branch  l 

U',  Posterior  cutaneous  branch r"  ""*'''■  '''^<'  "*"  fo'earm. 
IC,  Internal  cutaneous  nerve. 

E,  Anterior  or  external  branch. 

I,  Posterior  or  internal  branch  to  inner  side  of  forearm. 
SIC,  Small  cutaneous  nerve  (nerve  of  Wrisberg)  to  inner  side  of  arm. 
SSS,  Subscapular  nerves  : 

21,  Long  subscapular  nerve  to  latissimus  dorsi. 

21',  Muscular  branches  to  subscapularis  and  teres  major 

21",  Muscular  branches  to  subscapularis. 
C,  Circumflex  Nerce. 

sJ',  Branch  to  shoulder-joint. 

s,  Superior  division. 
7,  Cutaneous. 
"',  Muscular  to  deltoid. 

1,  Inferior  division. 
7",  Cutaneous. 
7'",  Muscular  to  teres  minor. 
3IS,  Muscitlo-qnral  Nerve. 

S,  Muscular  to  brachialis  anticus. 

8',  Muscular  to  triceps. 

8",  Muscular  to  anconeus. 

8"',  Muscular  to  supinator  longus. 

8"",  Muscular  to  supinator  brevis. 

SX,  Muscular  to  extensor  carpi  radialis  longior. 

icb,  Internal  cutaneous  branch  to  inner  side  of  arm. 

iiec,  Upper  external  cutaneous  branch  to  outer  side  of  arm. 

lee,  Lower  external  cutaneous  branch  to  outer  side  and  back  of  forearm. 

E,  Radial  nerve  cutaneous  to  dorsal  surface  of  thumb  and  two  outer  fingers. 

PI,  Posterior  Interosseous. 

9,  Muscular  branch  to  extensor  carpi  radialis  brevior. 

9',  Muscular  branch  to  extensor  ossis  metacarpi  poUicis. 

9",  Muscular  branch  to  extensor  primi  internodii  pollicis. 


388  ATEOPHIC    PARALYSES. 

10,  Muscular  branch  to  extensor  secundii  interuodii  poUicis. 

10',  Muscular  branch  to  extensor  indicis. 

10",  JIuscular  branch  to  extensor  carpi  ulnaris. 

(•  digitorum  communis  and  extensor 
10'",  Muscular  branch  to  extensor  |  mjuin^i  digiti. 
uj,  Branch  to  wrist-joint. 

M,  3Iedian  Nerve. 

11,  Muscular  branches  to  pronator  radii  teres. 

11',  Muscular  branches  to  flexor  profundus  digitonim. 

11",  Muscular  branches  to  flexor  longus  poUicis.  ' 

AI,  Anterior  interosseous  branch  to  pronator  quadratus. 

12,  Muscular  branch  to  flexor  carpi  radialis. 

12',  Musciilar  branch  to  flexor  sublimis  digitorum. 
12",  Muscular  branch  to  palmaris  longus. 

13,  Muscular  branch  to  opponens  poUicis. 
13',  Muscular  branch  to  abductor  pollicis. 

13",  Muscular  branch  to  flexor  breyis  pollicis  (outer  half). 

14,  Muscular  branch  to  first  lumbricalis. 
14',  Muscular  branch  to  second  lumbricalis. 
pc,  Palmar  cutaneous  branch. 

D  to  D4,  Digital  cutaneous  branches. 

U,  Ulnar  Nerve. 

ej,  Branch  to  elbow-joint. 

15,  Muscular  branch  to  flexor  profundus  digitorum  (inner  part). 
15',  Bluscular  branch  to  flexor  carpi  ulnaris. 

DC,  Dorsal  cutaneous  branch.     To  dorsal  surface  of  two  inner  fingers. 

2)'  e'.  Palmar  cutaneous  branch. 

c'.  Communicating  to  median. 

D3  to  D4,  Cutaneous  to  little  finger  and  inner  side  of  ring  finger. 

16,  Muscular  branches  to  palmaris  brevis. 

16',  Muscular  branches  to  abductor  minimi  digiti. 
10",  Bluscular  branches  to  opponens  minimi  digiti. 
16"',  Bluscular  branches  to  flexor  brevis  minimi  digiti. 

17,  IMuscular  branches  to  fourth  dorsal  interosseous. 
17',  Muscular  branches  to  third  dorsal  interosseous. 
17",  Muscular  branches  to  second  dorsal  interosseous. 
17'",  Muscular  branches  to  first  dorsal  interosseous. 

18,  Muscular  branches  to  third  palmar  interosseous. 
18',  Muscular  branches  to  second  palmar  interosseous. 
18",  Muscular  branches  to  first  palmar  interosseous. 

19,  Muscular  branches  to  fourth  lumbricalis. 
19',  Muscular  branches  to  third  lumbricalis. 

20,  Muscular  branches  to  adductor  i)ollicis. 

20',  Muscular  branches  to  flexor  brevis  pollicis  (inner  half). 

I 

tion  cannot  be  perceived,  but  the  epigastrium  may  be  felt  to  protrude 
slightly  during  expiration.  When  the  jjaralysis  is  unilateral  these 
signs  can  only  be  recognized  on  one  side.  The  breathing,  even  in  com- 
plete paralysis,  is  not  much  accelerated  during  rest,  but  dyspnoea  begins 
with  the  slightest  exertion,  and  the  respirations  frequently  rise  from 
forty  to  fifty  in  the  minute.  The  contents  of  the  bladder  and  rectum 
are  expelled  with  difficulty,  because  the  patient  is  unable  to  strain,  the 
action  of  the  abdominal  muscles  being;  rendered  ineffective  bv  the 
absence  of  the  counter-pressure  afforded  by  the  contracted  diaphragm. 


simple  neural  paralyses.  389 

8.  Paralysis  of  the  Muscles  Supplied  by  the  Brachial  Plexus. 

The  paralyses  of  the  brachial  plexus  may  be  divided  into  those,  a, 
of  the  muscles  of  the  neck  and  trunk,  and,  6,  those  of  the  upper 
extremity. 

a.   Paralysis  of  the  3Iuscles  of  the  Neck  and  Trunk. 

(1)  Paralysis  of  the  Pectoralis  Major  and  Pectoralis  Minor . — When 
these  muscles  are  paralyzed  the  power  of  adducting  the  arm  to  the 
thorax  or  of  resisting  passive  abduction  of  it  is  impaired  ;  the  patient  is 
unable  to  seize  the  opposite  shoulder  with  the  hand  ;  and  if  the  muscles 
are  likewise  atrophied  the  anterior  wall  of  the  axilla  is  reduced  to  a 
flaccid  fold  of  skin,  the  superior  ribs  and  intercostal  spaces  are  well 
marked,  and  the  subclavicular  fossa  is  deepened. 

(2)  Paralysis  of  the  rhomboid  muscles  of  the  levator  anguli  scapulce 
renders  forced  elevation  of  the  scapula  without  rotation  impossible. 

(3)  Paralysis  of  the  latissimus  dor  si  diminishes  the  power  of  adducting 
the  arm,  or  of  resisting  passive  abduction  of  it,  and  makes  it  difficult 
to  move  the  hand  to  the  buttock. 

(4)  Paralysis  of  the  outward  and  inivard  rotators  of  the  upper  arm 
is  readily  recognized  by  the  inability  of  the  patient  to  produce  out- 
ward or  inward  rotation  of  the  arm  respectively. 

(o)  Paralysis  of  the  serratus  magnus  is  often  preceded  by  neuralgic 
pains  in  the  neck  and  round  the  shoulder-blade;  the  scapula,  when  the 
arm  is  hanging  b}^  the  side,  is  somcAvhat  raised  and  approximated  to  the 
vertebral  column,  and  it  is  so  rotated  on  its  axis  that  its  inner  border  is 
directed  obliquely  upwards  and  outwards,  and  its  inferior  angle,  which 
stands  out  slightly  from  the  thoracic  wall,  is  drawn  close  to  the  vertebral 
column  (Fig.  116).  The  patient  experiences  difficulty  in  raising  the 
extended  arm  beyond  the  horizontal  level  because  the  usual  forward 
rotation  of  the  inferior  angle  of  the  scapula  is  not  affected,  but  by 
instinctively  leaning  the  body  to  the  opposite  side  he  can  raise  the  arm 
to  a  point  midway  between  the  horizontal  and  vertical  positions,  but  not 
further.  If  the  observer  rotates  the  scapula  forwards  and  fixes  the  bone 
in  that  position,  the  patient  is  enabled  to  raise  the  arm  to  a  vertical 
position.  When  the  arm  is  raised  to  a  horizontal  position  the  inner 
border  of  the  scapula  is  drawn  inwards  to  the  vertebral  column  while 
pushing  a  mass  of  muscle  before  it,  and  if  the  paralysis  be  bilateral  the 
inner  borders  of  the  scapula  may  actually  touch  one  another.  If  the 
raised  arm  be  brought  forwards,  the  inner  border  of  the  scapula  becomes 
more  and  more  separated  from  the  costal  wall,  so  that  a  deep  fossa  is 


390 


ATROPHIC    PARALYSES, 


formed  in  which  the  hand  may  easily  be  laid  so  as  to  feel  the  inner 
surface  of  the  bone,  and  if  the  paralysis  be  bilateral  the  scapulae  enclose 
a  deep  hollow  in  which  the  muscular  bellies  of  the  rhomboid  muscles 
may  be  seen  to  project.  The  patient  experiences  difficulty  in  crossing 
the  arms  in  front  of  the  chest,  and  in  moving  the  apex  of  the  shoulder 

Fig.  116. 


forwards  as  in  delivering  a  blow  in  fencing,  and  he  offers  less  resistance 
than  in  health  to  forcible  retraction  of  the  shoulder.  The  chest  expands 
less  and  the  digitations  of  the  serratus  magnus  with  the  external  oblique 
are  not  so  marked  on  the  paralyzed  as  on  the  healthy  side  during  forced 
inspiration. 


b.  Paralysis  of  the  Muscles  of  the  Upper  Extremity. 

(1)  Paralysis  of  the  Circumflex  Nerve.  —  The  circumflex  ner\e 
supplies  the  deltoid  and  the  teres  minor  muscles,  but  the  symptoms  are 
almost  exclusively  those  of  paralysis  of  the  deltoid.  The  arm  cannot 
be  raised  outwards  or  forwards,  and  during  attempts  to  raise  it  the 
deltoid  remains  quite  relaxed,  and  the  arm  hangs  helpless  along  the  side 


SIMPLE    NEURAL    PAEALYSES.  391 

of  the  thorax.  The  muscle  frequently  undergoes  atrophy,  and  the 
slioulder-joint  becomes  so  loose  that  a  deep  groove  can  be  felt  throucrh 
the  atrophied  muscle  between  the  head  of  the  humerus  and  the  glenoid 
cavity.  There  may  be  pain  in  the  shoulder-joint  and  in  the  substance 
of  the  muscle,  but  other  sensory  disturbances  in  the  region  of  distribu- 
tion of  the  nerve  are  rare.  Lesions  of  the  circumflex  nerve  do  not  give 
rise  to  any  very  manifest  disorders  of  sensibility,  but  there  may  be  a 
slight  degree  of  1)lunting  of  sensibility  on  the  outer  surface  of  the 
shoulder  (Figs.  120,  121). 

(2)  Paralysis  of  the  MuscuJo-cutaneous  JVerve. — Paralysis  in  the 
region  of  distribution  of  this  nerve  greatly  diminishes  the  power  of 
flexing  the  forearm  upon  the  arm,  especially  when  the  forearm  is  supi- 
nated  so  that  the  flexor  action  of  the  supinator  longus  can  no  lon»er 
come  into  play.  Paralysis  of  the  musculo-cutaneous  nerve  is  accom- 
panied by  anaesthesia  along  the  radial  border  of  the  forearm  (Fio-s.  120, 
121). 

(3)  Paralysis  of  th'  Musculo-spiral  N<rve. — Paralysis  of  this  nerve 
is  frequently  caused  by  injury  of  the  nerve  as  it  winds  round  the 
humerus.  The  most  frequent  cause  of  injury  is  compression  of  the 
nerve  between  the  bone  and  some  hard  substance  during  the  deep  and 
prolonged  sleep  which  follows  intoxication.  The  nerve  may  also  be 
subjected  to  pressure  in  the  axilla  by  means  of  improperly  constructed 
crutches.  AVhen  the  nerve  is  completely  paralyzed  the  hand  is  main- 
tained in  a  flexed  position,  and  hangs  helpless  when  the  forearm  is 
extended  and  pronated.  The  patient  is  unable  to  raise  the  hand  or 
extend  the  fingers  at  the  metacarpo-phalangeal  joints;  the  thumb  is 
flexed  and  adUucted,  and  the  fingers  are  flexed  over  the  thumb.  When 
the  hand  is  placed  on  a  table  it  cannot  be  raised  or  moved  laterally,  but 
the  lateral  movements  of  the  fingers  remain  unimpaired.  The  patient 
is  unable  to  supinate  the  forearm,  especially  when  it  is  extended  so  as 
to  exclude  the  action  of  the  biceps*  Paralysis  of  the  supinator  longus 
is  readily  recognized  by  requesting  the  patient  to  make  a  powerful  effort 
to  flex  the  arm  against  a  resisting  object  when  the  forearm  is  maintained 
in  a  half-flexed  position  and  midway  between  pronation  and  supination  : 
it  is  then  found  that  the  muscle  does  not  enter  into  contraction  but 
remains  flaccid  and  soft.  In  lead  paralysis  the  supinator  longus  is 
always  spared  unless  the  paralysis  implicates  the  deltoid  and  biceps : 
Avhen  the  lesion  is  situated  in  the  nerve  as  it  winds  round  the  humerus 
the  triceps  muscle  is  spared,  but  in  crutch  paralysis  it  is  paralyzed  and 
the  patient  cannot  extend  the  forearm  upon  the  arm.  The  action  of 
the  flexor  muscles  is  apparently  weakened,  but  this  is  due  to  the  fact 
that  the  flexed  position  assumed  hx  the  hand  approximates  the  points 


392 


ATROPHIC    PARALYSES. 


of  origin  and  insertion  of  these  muscles.  Disease  of  the  musculo-spiral 
nerve  when  situated  high  up  gives  rise  to  anaesthesia  in  the  areas  of 
distribution  of  the  superior  and  inferior  external  cutaneous  branches 
(Figs.  120,  121,  I'CB,  ECB) ;  but  when  the  lesion  is  situated  low 


Fig.  118. 


Fig.  119. 


Fig.  117. — Distrirutiok  op  the  Sensory  Nerves  on  the  Back  ok  the  IlAvn.  (After  Kr.^vse  ) 
r,  Radial ;  m,  median ;  and  u,  ulnar  nerve. 

Fig.  118.— Showing  the  Distribution  of  the  Anj:sthesia  in  a  Case  of  Division  of  the  JIusi.ulo- 
SPIRAL  Nerve  in  the  Arm.  (After  LiTifcvANT.)  A,  Deeply  shaded,  to  show  the  area  of  greatest  anaes- 
thesia ;  B,  shaded  in  a  medium  degree,  to  show  the  area  of  partial  anaesthesia ;  C,  faintly  shaded,  to  show 
the  area  of  slight  anjesthesia. 

Fig.  119.— The  Dorsal  Aspect  of  the  Hand  Two  Weeks  after  Resection  of  the  Radial  Nerve. 
(After  Mitchell.)  A  B  and  A  C,  the  length  of  the  portion  removed.  The  light  shading  represents  the 
area  in  which  tactile  sensibility  was  diminished  ;  the  deep  shading  the  area  in  wliich  it  was  lust. 

down,  the  dorsal  surfaces  of  the  thumb  and  of  the  inde.x  and  half  of  the 
middle  finger  as  far  as  to  the  second  phalanx  and  the  corresponding 
parts  of  the  back  of  the  hand  are  alone  affected  (Fig.  117,  r).     A  slight 


SIMPLE    XEURAL    PARALYSES, 


393 


degree  of  anesthesia  may  sometimes  be  found  over  the  back  of  all  the 
fingers,  including  the   little   finger,  which   is  supposed  to  be  entirely 


Fig.  120. 


Fig.  12  L 


Figs.  120  and  121.— Citaneous  Nerves  of  the  Trunk  .\nd  Upper  Extremity.     (After  Flower.) 
Su,  Supraclavicular  nerve. 
IID,  Second  dorsal. 

PS,  Posterior  branches  of  the  spinal  nerves. 
LI,  Lateral  branches  of  the  intercostal  nerves. 
AI,  Anterior  branches  of  the  intercostal  nerves. 
II,  Iliac  branch  of  ilio-inguinal  nerve. 
I'H',  Ilio-hypogastric  nerve. 
C,  Circumflex  nerve. 
IH,  Intercostal  humeral. 
AV,  Nerve  of  Wrisberg. 

I'CB,  Internal  cutaneous  branch  of  musculo-spiral  nerve. 
ECB,  External  cutaneous  branch  of  musculo-spiral  nerve. 
ICB,  Internal  cutaneous  nerve. 
MB,  JIusculo-cutaneous  nerve. 
R,  Radial  nerve. 
U,  Ulnar  nerve. 
M,  Median  nerve. 

innervated  by  the  ulnar  nerve.     This  fact  is  well  illustrated  by  a  ca.se 
reported  by  Letievant,  in  which  the  nerve  was  divided  in  the  inferior 


894 


ATROPHIC    PARALYSES. 


and  internal  aspect  of  the  left  arm,  and  the  distribution  of  the  anaesthesia 
two  and  a  half  years  after  the  injur}^  is  shown  in  Fig.  118.  In  most 
cases,  however,  the  area  of  anesthesia  is  much  more  limited  than  the 
anatomical  distribution  of  the  nerve  would  lead  us  to  expect.  A  case 
is  reported  by  S.  Weir  Mitchell  in  which  three  inches  of  the  radial  nerve 
were  removed  in  the  back  of  the  forearm,  and  the  distribution  of  the 
anesthesia  as  it  was  found  two  weeks  after  the  operation  is  shown  in 
Fig.  119. 

(4)  Paralysis  of  the  median  nerve  abolishes  the  power  of  pronating 
the  hand  and  of  closing  the  hand  to  grasp  an  object,  with  the  exception 
of  the  two  ulnar  fingers,  which  can  still  be  partially  flexed,  because  the 

Fig.  123. 


Figs.  122  and  12S. — Radial  Bokher  and  Dorsal  Aspect  hfthe  Hand,  showing  the  Distkibl'tiov  ok 

An.esthesia  in  a  Case  of  Division  of  the  Median  Nerve.     (After  LfeTifevANT.) 

A,  Deep  shading  representing  more  or  less  complete  anaesthesia  ;  B,  E,  and  H,  light  shading,  and 

C,  medium  shading,  representing  a  slight  and  medium  degree  of  antesthesia  respectively. 

flexor  profundus  digitorum  is  in  part  supplied  by  the  ulnar  nerve.  The 
patient  is  unable  to  abduct,  oppose,  or  perform  any  of  the  more  delicate 
movements  of  the  thumb,  which  is  permanently  extended  and  adducted. 
while  its  metacarpal  bone  is  drawn  backwards  so  that  it  lies  on  a  plane 


SIMPLE    XEURAL    PARALYSES. 


395 


with  the  metacarpal  bones  of  the  fingers,  as  in  the  hand  of  the  monkey. 
Flexion  at  the  wrist  is  accompanied  by  adduction,  owinor  to  the  un- 
opposed action  of  the  flexor  carpi  ulnaris.  Flexion  of  the  first  with 
extension  of  the  second  and  third  phalanges  of  the  fingers  can  be  effected 
by  means  of  the  interossei ;  and,  indeed,  the  last  two  phalanges  may 
be  hyperextended  owing  to  the  unopposed  action  of  these  muscles.  The 
muscles  of  the  forearm  and  ball  of  the  thumb  become  atrophied  in 
severe  cases. 

The  sensory  disorders  are,  according  to  Letievant,  distributed  over 
the  palmar  surfaces  of  the  thumb,  index,  and  radial  border  of  the  middle 
finger,  the  thenar  eminence,  and  the  radial  half  of  the  palm,  and  over 
the  dorsal  surfaces  of  the  ungual  and  middle  phalanges  of  the  index 
and  middle  fingers  and  occasionally  the  ungual  phalanx  of  the  thumb 
(Figs.  122,  123).  The  anaesthesia  is  partial  everywhere  except  over 
the  palmar  surface  of  the  whole  of  the  ungual  phalanx  of  the  index 

Fig.  124. 


SHOWING  THE  DISTRIBUTION  OF  THE  An.BSTHESIA  ON  THE  BaCK  OF  THE  FiNGEBS  IN  A  CaSE  (jF 

Injtjry  of  the  3IEDIAN  Xerve.     (After  Bernhardt.) 


finger,  and  part  of  the  dorsal  surfiice  of  the  same  phalanx.  The  different 
degrees  of  shading  in  Figs.  122  and  123  represent  the  varying  degrees  of 
anaesthesia,  the  very  deep  shading  at  A  representing  complete  anaesthesia. 
A  case  is  reported  by  Bernhardt  in  which  the  median  nerve  was  para- 
lyzed as  the  result  of  an  injury.  Four  months  after  the  injury  the 
sensibilitv  of  the  skin  of  the  ball  of  the  thumb  and  the  i-adial  half  of 


896 


ATROPHIC    PARALYSES, 


the  palm  was  somewhat  diminished,  whilst  that  of  the  palmar  aspect  of 
the  thumb,  index,  middle,  and  radial  border  of  the  ring  finger  was 
greatly  lessened,  the  loss  of  sensibility  becoming  progressively  greater 
from  the  basal  to  the  ungual  phalanges.  On  the  dorsal  aspect  the  sen- 
sibility of  the  skin  of  the  thumb  and  little  finger  was  intact  over  all 
the  phalanges,  but  was  much  diminished  over  both  borders  of  the  middle 
and  ungual  phalanges  of  the  index  and  middle  fingers,  and  over  the 
radial  border  of  the  corresponding  phalanges  of  the  ring  finger  (Fig.  124). 
In  many  cases  of  paralysis  of  the  median  nerve,  however,  the  distribu- 
tion of  the  anaesthesia  is  by  no  means  so  extensive  as  it  was  in  the  cases 
of  Letievant  and  Bernhardt. 

(5)  Paralyds  of  the  ulnar  nei've  limits  the  power  of  ulnar  flexion 
and  adduction  of  the  hand,  and  abolishes  the  power  of  completely 
flexing  the  last  two  fingers,  of  moving  the  little  finger,  of  separating 
the  fingers  from  and  compressing  them  against  the  middle  finger,  and 

Fig.  12.). 


1-  Main  en  Griffe.  2. 

(1)  Hand,  Palmar  Surface.    (2)  Dorsal  Surface.    (After  Dvchexxe.) 

A,  Wouml  of  the  ulnar  nerve  ;  B,  Ends  of  the  metacarpal  bones  ;  D,  Tendons  of  the  flexor 

sulilimis  ;  (',  Muscles  of  the  ball  of  the  thumb. 

of  flexing  the  first  and  extending  the  second  and  third  phalanges  of  all 
the  fingers.  The  patient  is  also  unable  to  adduct  the  thumb  and  apply 
It  firmly  to  the  metacarpal  bone  of  the  index  finger.  If  the  interossei  and 
lumbricales  are  alone  paralyzed,  the  combined  traction  of  the  extensors 


.SIMPLE    NEURAL    PAKALYSES. 


597 


and  flexors  of  the  fingers  produces  hyiDerextension  of  tlie  first  and 
flexion  of  the  last  two  phalanges,  and  the  hand  assumes  the  chiAv-like 
appearance  which  is  so  characteristic  of  paralysis  of  the  ulnar  nerve 
above  the  wrist,  and  of  certain  cases  of  progressive  muscular  atrophv. 
In  severe  and  protracted  cases  the  first  phalanges  are  dislocated  backr 
wards  upon  the  metacarpal  bones  by  the  unantagonized  action  of  the 
extensors  of  the  fingers ;  the  second  phalanges  become  dislocated  for- 
wards on  the  first,  and  the  third  on  the  second  from  the  unantagonized 
action  of  the  flexor  digitorum  sublimis  and  profundus,  respectively,  and 
then  the  most  characteristic  form  of  the  claw-hand  (warn  en  griffe)  is 
produced  (Fig.  125).  The  accompanying  atrophy  of  the  muscles  gives 
to  the  hand  some  of  its  chief  characteristics.  The  hypothenar  eminence 
is  flattened  from  atrophy  of  the  muscles  of  the  little  finger,  deep  furrows 


Fig.  ]2(j. 


Fig.  12 


A,  Deep  shading,  representing  complete  anwstliesia ;  B,  liglit  shading,  represents  slight,  and 
C,  medium  sliading,  represents  a  medium  degree  of  anaesthesia.     (After  L£ti£va.nt.) 


appear  between  the  metacarpal  bones  from  atrophy  of  the  interossei : 
the  metacarpal  bone  of  the  index  finger  may  be  felt  immediately  under- 
lying the  skin  from  disappearance  of  the  abductor  indicis :  and  when 
the  mass  of  tissue  Avhich  lies  between  the  metacarpal  bones  of  the  thumb  _ 


398  ATROPHIC    PARALYSES. 

and  index  finger  is  grasped  by  tlie  observer  it  is  felt  to  consist  of  little 
more  than  a  fold  of  skin,  owing  to  atrophy  of  the  adductor  pollicis  and 
inner  head  of  the  adductor  brevis  pollicis. 

The  senso7-y  disorders  appear  on  the  palmar  and  dorsal  aspects  of  the 
little  and  half  of  the  ring  finger,  and  the  corresponding  part  of  the 
palm  and  back  of  the  hand,  but  the  aniesthesia  is  only  complete  over 
a  very  limited  portion  of  the  ulnar  border  of  the  hand  (Figs.  126, 127). 
All  severe  lesions  of  the  ulnar  nerve  are  apt  to  give  rise  to  glossy  fingers, 
and  various  other  trophic  phenomena. 

(6)  Combined  Paralysis  of  the  Nerves  of  the  Brachial  Plexus. — 
Various  kinds  of  paralysis  occur  after  dislocation  of  the  shoulder-joint. 

In  suhcoracoid  luxations  the  subjacent  nerve  trunks  are  especially 
liable  to  injury,  and  the  Avhole  of  the  nerves  may  be  compressed  or 
lacerated. 

In  fracture  of  the  humerus  one  or  more  nerve  trunks  may  be  injured, 
or  may  afterwards  be  implicated  in  the  formation  of  callus.  The  mus- 
culo-spiral  is  the  most  frequently  paralyzed,  then  the  ulnar,  and  more 
rarely  the  median  nerve. 

In  dislocations  and  fractures  near  the  elbow-joint  the  ulnar  and 
median  nerves  are  liable  to  be  affected. 

Tight  bandaging  may  also  give  rise  to  a  widely  distributed  and 
obstinate  paralysis. 

In  all  these  forms  of  paralysis  recovery  is  slow,  the  reaction  of  degen- 
eration is  manifested  in  the  affected  nerves  and  muscles,  and  many  of 
them  prove  incurable. 

(7)  Paralysis  of  the  Muscles  Supplied  by  the  Fifth  Cervical  Nerve. 
— The  root  of  the  fifth  cervical  nerve  is  liable  to  suffer  injury  from 
various  causes  as  it  descends  over  the  transverse  processes  of  the  fifth 
and  sixth  cervical  vertebrae  to  join  the  brachial  plexus!  It  may  be 
compressed  by  a  tumor  in  this  course,  but  more  frequently  the  nerve  is 
suddenly  injured  by  accident  at  this  point.  In  accidents  which  have 
given  rise  to  this  injury,  the  upper  extremity  has  been  directed  forwards 
and  upwards  to  break  a  fall,  and  in  such  a  position  that  when  the  col- 
lision comes  the  clavicle  is  thrust  upwards  and  backwards,  and  conse- 
(juently  the  root  of  the  fifth  nerve  may  receive  a  ^'iolent  blow  as  it 
passes  over  the  transverse  processes  of  one  of  the  vertebrae.  The  first 
suggestion  of  this  exijlanation  came  from  Mr.  Williamson,  one  of  the 
house  physicians  at  the  Royal  Infirmary,  and  the  proljabilities  of  it 
were  subsequently  verified  on  the  dead  subject  by  Mr.  Collier,  Demon- 
strator of  Anatomy  at  Victoria  University.  The  muscles  which  are 
paralyzed  after  this  injury  are  the  deltoid,  biceps,  brachialis  anticus, 
and  supinators  of  the  forearm,  and  to  a  less  degree  the  outward  rotators 


SIMPLE    NEURAL    PARALYSES, 


899 


(.f  the  humerus.  The  sensory  disorders  consist  of  formication  and 
numbness  in  the  outer  surfaces  of  the  arm,  forearm,  thumb,  and  index 
finger.  The  same  muscles  are  paralyzed  in  the  form  of  paralysis  de- 
scribed by  Duchenne  under  the  name  of  obstetrical  infantile  paralysis 
of  the  superior  extremities.  It  is  caused  by  turning  or  some  other 
operative  procedure  during  delivery. 

(8)  Paralysis  of  the  Inferior  Roots  of  the  Brachial  Plexus.— 
Paralysis  of  the  roots  of  the  eighth  cervical  and  first  dorsal  nerves  is 
observed  in  cases  of  pachymeningitis  cervicalis  hypertrophica  when  the 
lesion  is  situated  on  a  level  with  the  junction  of  the  cervical  and  dorsal 
regions  of  the  cord.  The  muscles  supplied  by  the  ulnar  and  median 
nerves  are  then  paralyzed,  while  those  supplied  by  the  musculo-spiral 
nerve  remain  comparatively  free,  and  consequently  the  hand,  especially 
when  the  patient  tries  to  grasp,  assumes  the  claw  form  shoAvn  in  Fio-. 
128.     In  most  cases  the  second  dorsal  nerve  is  likewise  implicated  in 


Fig.  128. 


Attitude   of  the  Hand   ix   PACHiMrMM.iii^   iii\iiaii>   Il^rERTKOPHicA,    when   the  disease  is 

SITUATED   ON   A   LEVEL   WITH    THE    LOWER    HALF    OF    THE    CERVICAL    ENLAEOEJIENT    OF    THE    SPINAL  CORP. 

(.\fter  Charcot.) 

the  lesion  and  consequently  the  anaesthesia  caused  by  implication  of 
the  posterior  roots  is  found  in  the  area  of  distribution  of  the  intercosto- 
humeral,  the  nerve  of  Wrisberg,  the  large  internal  cutaneous,  and  the 
terminal  cutaneous  branches  of  the  ulnar  nerve.  In  pachymeningitis 
the  sensory  conducting  paths  are  often  implicated,  and  the  whole  of 
the  body  below  the  level  of  the  lesion  is  then  anaesthetic,  as  is  shown 
in  Fig.  129.  In  a  case  of  tubercular  tumor  of  the  sninal  membranes 
which  involved  the  roots  of  the  seventh  and  eighth  cervical  and  first 
dorsal  nerves — the  posterior  root  of  the  seventh  cervical  was  not  much 
implicated — the  anaesthesia  was  distributed  as  is  shown  in  Fig.  130. 

(9)  Rupture  of  the  Brachial  Plexus. — Rupture  of  the  brachial  plexus 
has  generally  been  caused  by  the  patient  falling  from  a  height  and  grasp- 


400 


ATROPHIC    PARALYSES. 


ing  some  object  during  his  fall,  by  severe  pulling  of  the  arm,  or  by  the 
fall  of  a  heavy  weight  on  the  shoulder.  Immediately  after  the  accident 
all  the  muscles  of  the  upper  extremity  are  paralyzed.  The  latissimus 
dorsi  and  the  lower  two-thirds  of  the  pectoralis  major  are  also  paralyzed  ; 
but  the  upper  third  of  the  pectoralis  major,  the  pectoralis  minor,  and 
the  internal   and  external  rotators  of  the  humerus  are  unaffected,  but 


Fig.  130. 


Fig.  120. — The  shaded  portion  shows  the  distribution  of  iiiuvsthesia  in  u  cajse  of  cervical  pachymeningitis, 
in  which  the  lesion  was  situated  on  a  level  with  the  eighth  cervical  and  first  and  second  dorsal  nerves. 

Fig.  130 — The  shaded  portion  shows  the  distribution  of  anesthesia  in  a  case  in  which  a  tubercular 
tumor  was  situated  on  a  level  with  the  roots  of  the  seventh  and  eighth  cervical  and  first  dorsal  nerves. 

the  serratus  magnus  may  be  relatively  feeble,  although  not  completely 
paralyzed.  In  a  case  under  my  care,  however,  the  latissimus  dorsi,  the 
deltoid,  biceps,  brachialis  anticus,  and  the  supinators  of  the  forearm 
were  found  to  have  completely  recovered  when  the  i)atient  Avas  exam- 
ined eighteen  months  after  the  accident,  although  these  muscles  were 
known  to  have  remained  completely  paralyzed  for  eight  months.  Oculo- 
pupillary  phenomena  are  always  observed  in  rupture  of  the  brachial 
plexus.     On  the  affected  side  there  are  paralytic  myosis,  diminution  of 


SIMPLE    NEURAL    PARALYSES. 
Fig.  L3L  Fig.  132. 


401 


Figs.  131  ami  132. — Posterior  and  anterior  aspect  respectively  of  the  arm  in  a  case  of  rupture  of  the 
brachial  plexus,  the  shaded  area  showing  the  distribution  of  the  anasothesia.  By  an  oversight  the  right 
arm  is  represented  as  being  affected  instead  of  the  left. 


Fig.  133. 


The  line  a  a  a,  ou  the  outer  surftice  of  the  arm,  marks  the  lioundary  above  and  outside  of  which  sensation 
is  preserved.     The  dotted  line  6  6  marks  the  same  for  the  inner  surface  of  the  arm.     (After  Maurv  and 

Dtjhring.) 

26 


402  ATROPHIC    PARALYSES. 

the  palpebral  fissure,  and  often  relative  elevation  of  temperature  in  the 
external  meatus  of  the  ear.  The  area  of  absolute  anaesthesia  in  the 
case  observed  by  me  is  shown  in  Figs.  131  and  132.  There  was  a  rela- 
tive diminution  of  tactile  sensibility  over  the  whole  of  the  skin  of  the 
upper  arm.  The  sensation  to  the  inner  surface  of  the  arm  would  be 
probably  supplied  by  the  intercosto-humeral  nerve,  which  would  remain 
uninjured  in  this  affection.  In  a  case  of  excision  of  the  brachial  plexus 
by  Maury  and  Duhring  the  sensations  of  pain  and  touch  were  absent, 
six  months  after  the  operation,  over  the  whole  of  the  hand  and  forearm, 
and  over  the  anterior  aspect  of  the  arm  as  represented  in  Fig.  133,  a  a. 
In  this  case  the  communicating  branch  from  the  fourth  and  the  fibres 
derived  from  the  fifth  cervical  root  would  be  divided,  while  in  rupture 
these  fibres  had  been  uninjured  from  the  first  or  had  recovered. 


9.  Paralysis  of  the  Muscles  Supplied  by  the  Dorsal  Nerves. 

a.  Paralysis  of  the  Respirdtory  Muscles. 

(1)  Complete  paralysis  of  the  respiratory  muscles  occurs  when  the 
respiratory  centres  in  the  medulla  oblongata  are  affected,  or  when  the 
motor  tracts  proceeding  from  these  centres,  and  which  run  in  the  lateral 
columns  of  the  cord,  are  interrupted.  In  these  cases  rapid  death  is 
inevitable. 

(2)  Unilateral  paralysis  of  the  respiratory  muscles  does  not  imme- 
diately endanger  life.  This  fi)rm  of  paralysis  may  be  caused  by 
unilateral  lesions  of  the  spinal  cord,  but  cerebral  disease  does  not  inter- 
fere much  with  the  respiratory  process. 

(3)  Peripheral  paralysis  of  the  respiratory  muscles  only  affects  indi- 
vidual muscles  or  a  group  of  muscles,  and  paralysis  of  one  or  two  of 
the  intercostal  muscles  is  not  readily  distinguished. 


h.  Paralysis  of  the  Dorsal  and  Abdominal  Muscles. 

The  extensors  of  the  back  are  not  infrequently  more  or  less  para- 
lyzed. Spinal  curvatures  are  often  caused  in  young  people  by  a  rela- 
tive feebleness  of  the  dorsal  muscles  of  one  side.  Paralysis  of  these 
muscles  may  be  caused  by  rheumatism  and  injuries  of  the  back,  and 
by  spinal  disease,  such  as  acute  atrophic  spinal  paralysis  and  all  the 
forms  of  ascending  myelitis  and  progressive  muscular  atrophy,  while  it 
gives  to  pseudo-hypertrophic  paralysis  one  of  its  most  characteristic 
features. 


SIMPLE    NEURAL    PARALYSES.  403 

(1)  Bilateral  paralysis  of  the  extensors  of  the  dorsal  region  gives 
rise  to  a  large  and  equable  curve  of  the  vertebral  column ;  the  patients 
are  bent  and  doubled  up  as  in  old  age,  and  are  unable  to  hold  them- 
selves erect,  but  passive  straightening  of  the  vertebral  column  can 
easily  be  effected,  and  this  distinguishes  paralytic  kyphosis,  as  the  con- 
dition is  called,  from  the  kyphosis  which  results  from  muscular  con- 
tracture or  disease  of  the  vertebrae. 

(2)  Unilateral  paralysis  of  the  dorsal  muscles  gives  rise  to  the 
various  forms  of  paralytic  scoliosis. 

(3)  Bilateral  paralysis  of  the  extensors  of  the  lumbar  region  pre- 
sents very  characteristic  features — the  lumbar  vertebrae  are  arched  for- 
Avards,  forming  a  hollow  in  the  back  which  is  increased  by  the  upper 
part  of  the  body  being  thrown  backwards  in  order  to  compensate  for 
the  incurvation  of  the  lumbar  portion.  A  plumb  line  allowed  to  drop 
from  the  most  prominent  spinous  process  of  the  dorsal  vertebra  clears 
the  sacrum  generally  by  one  or  two  inches. 

(4)  Paralysis  of  the  abdominal  muscles  is  rare  as  an  isolated  affec- 
tion, but  is  common  as  a  symptom  of  spinal  paralysis,  and  occurs  occa- 
sionally in  progressive  muscular  atrophy.  Bilateral  paralysis  of  the 
abdominal  muscles  renders  all  expiratory  efforts  like  coughing  and 
singing  ineffective.  The  power  of  compressing  the  abdomen  is  im- 
paired, and  consequently  diflSculty  is  experienced  in  evacuating  the 
contents  of  the  bladder  and  rectum.  The  abdomen  is  large  and  protu- 
berant, its  walls  are  relaxed,  and  the  patient  is  unable  to  raise  the  upper 
part  of  the  body  from  the  recumbent  position,  or  to  sit  up  in  bed  without 
being  propped  up  with  the  hands.  In  walking  or  standing  the  upper 
part  of  the  body  is  bent  slightly  forwards  and  balanced  exclusively  by 
the  lumbar  muscles,  and  consequently  each  backward  movement  of  the 
centre  of  gravity  renders  the  patient  liable  to  fall  on  his  back,  because 
the  abdominal  muscles  are  incapable  of  drawing  the  body  forwards.  A 
plumb  line  let  fall  from  the  most  prominent  of  the  spinous  process  of 
the  vertebrae  falls  well  within  the  sacrum.  If  the  lower  extremities  are 
paralyzed,  this  symptom  cannot  be  determined. 

In  unilateral  paralysis  of  the  abdominal  muscles  the  umbilicus  is 
carried  to  the  sound  side  with  each  movement  of  forcible  expiration, 
and  during  the  act  of  straining. 

I'O.  Paralysis  of  the  Muscles  Supplied  by  the  Lumbar  Plexus. 

a.  Paralysis  of  the  anterior  crural  nerve  (Fig.  134,  AC)  arises  from 
injuries  of  the  vertebral  column  and  pelvis,  tumors,  and  extravasation 
of  blood  in  the  cauda  equina,  inflammation  of  the   knee-joint,  psoas 


404 


ATEOPHIC    PARALYSES. 


abscess,  fracture  of  the  thigh,  dislocation  of  the  hip-jomt,  wounds 
and  injuries  of  the  lower  abdominal  and  crural  regions,  pelvic  and 
crural  tumors,  and  neuritis,  while  it  is  a  frequent  symptom  of  all  forms 
of  spinal  paralysis. 


Fig.  134. 


LusiBAR  Plexus. 
XL,  IIL,  IIIL,  and  IVL.— The  first,  second,  third,  and  fnurth  hiiuliHr  nerves,  respectively. 
D,  Communicating  branch  from  the  last  dorsal  nei-ve. 
CCCC,  Posterior  cutaneous  branches. 
mmmni,  Branches  to  the  muscles  of  the  back. 
IH,  Ilio-hypogastric  nerve. 

I,  Iliac  branch,  cutaneous,  to  surface  of  gluteal  region. 
H,  Hypogastric  branch,  cutaneous,  to  surface  of  hypogastric  region. 

1,  Muscular  branch  to  obliquus  internus. 

T,  Rectus  abdominis. 


simpi.p:  neural  paralyses.  405 

II,  lliu-iDguinal  nerve,  cutaneous,  to  inguinal  region  ami  scrotum. 
UC,  Genito-crural  nerve. 

6,  (Jenital  branch  to  spermatic  cord  or  round  ligament. 
2,  Muscular  branch  to  cremaster. 

C,  Crural  branch,  cutaneous,  to  surface  of  upper  part  of  front  of  thigh. 
EC,  External  cutaneous. 

P,  Posterior  brancli,  cutaneous,  to  upper  and  outer  part  of  thigli. 

A,  Anterior  branch,  cutaneous,  to  front  of  thigh. 

ps,  3Iuscular  branches  to  psoas  muscle. 
AC,  Anterior  crural  nerve. 

3,  Muscular  branches  to  iliacus. 
3'  3Iuscular  branches  to  sartorius. 
3",  3Iuscular  branches  to  pectineus. 
fa,  Branch  to  femoral  artery. 

3IC,  Middle  cutaneous  to  front  of  thigh. 

IC,  Internal  cutaneous  to  inner  part  of  thigh  and  leg. 

LS,  Internal  or  long  saphenous. 

0,  Cutaneous  over  inner  ankle. 

/',  Cutaneous  to  inner  side  of  foot. 

4,  3Iuscular  branch  to  rectus  femorls. 
4',  Muscular  branch  to  vastus  externiis. 
4",  Jluscular  branch  to  crureus. 

4'",  Muscular  branch  to  subcrureus. 
4"",  JIuscular  branch  to  vastus  internus. 
Kj,  Branch  to  knee-joint. 
0,  Obturator  nerve. 

hj,  Branch  to  hip-joint. 

c'.  Communicating  with  branches  of  internal  cutaneous  and  internal  saphenous. 

5,  Muscular  branch  to  pectineus. 

5',  Muscular  branch  to  obturator  externus. 

6,  Muscular  branch  to  adductor  longus. 
6',  Muscular  branch  to  gracilis. 

C",  Muscular  branch  to  adductor  brevis. 
6'"  6"",  Muscular  branch  to  adductor  magnus. 
Kj',  Branch  to  knee-joint. 
L,  Communicating  branch  to  fifth  lumbar  nerve. 

Symptoms. — The  patient  is  unable  to  flex  the  leg  at  the  hip-joint  or 
raise  the  body  from  the  recumbent  position.  He  cannot  extend  the 
leg,  and  when  sitting  he  is  unable  to  move  the  leg  forwards.  Standing 
and  sitting  upright  are  rendered  insecure,  while  walking,  jumping, 
and  running  are  difficult  or  impossible,  and  the  difficulty  is  much 
increased  when  both  nerves  are  affected. 

The  sensory  disorders  extend  over  the  lower  two-thirds  of  the  thigh, 
the  reo-ion  of  the  knee,  and  the  inner  side  of  the  leg  and  foot. 

h.  Paralysis  of  the  obturator  nerve  (Fig.  134,  0)  may  be  caused  by 
strangulated  obturator  hernia,  and  the  pressure  of  the  head  of  the 
child,  or  of  obstetric  instruments,  in  difficult  deliveries. 

Symptoms. — The  patient  is  incapable  of  adducting  the  thigli,  of 
pressing  the  knees  together,  or  of  crossing  one  leg  over  the  other.  Out- 
ward rotation  of  the  thigh  is  rendered  difficult,  and  the  affected  leg  soon 
tires  in  walking.  A  slight  degree  of  anaesthesia  extends  down  the  inner 
side  of  the  thigh  as  far  as  the  knee. 


406 


ATROPHIC    PAEALYSES. 


c.  Paralysis  of  the  gluteal  nerves  (Fig.  135,  SG)  is  caused  by  tumors 
and  lesions  of  the  cauda  equina,  fractures  of  the  sacrum  and  pelvis,  and 
various  diseases  of  the  spinal  cord. 


Fig.  135. 


Sacral  and  Coccygeal  Nerves. 
VL,  IS,  IIS,  HIS,  IVS,  VS,  VIS.— Fifth  hiinbar,  and  fiist,  sccoml,  third,  fourth,  fifth,  and  .sixth 

sacral  nerves. 
LS,  Lumbo-sacral  cord. 

c,  c.  Posterior  cutaneous  nerves. 

TO,  Branches  to  muscles  of  back. 

1,  Branches  to  pyriformis  muscle. 

3,  Muscular  branches  to  obturator  internus. 


SIMPLE    XEURAL    PARALYSES.  407 

3',  JIuscular  branches  to  gemellus  superior. 
3'',  Muscular  branches  to  gemellus  inferior. 
3'",  Muscular  branches  to  quadratus  femoris. 
SG,  Superior  gluteal  nerve. 

2,  Muscular  branches  to  gluteus  medius. 

2',  Sluscular  branches  to  gluteus  minimus. 

2",  Muscular  branches  to  tensor  vaginte  femoris. 

12,  Muscular  branches  to  gluteus  maximus. 
I  G,  Inferior  gluteal  nerve  (cutaneous). 

I  P,  Inferior  pudendal  nerve,  cutaneous,  to  perineum  and  scrotum,  or  external  labium. 
C,  Cutaneous  branch  to  back  of  thigh  and  upper  part  of  leg. 
P,  Pudic. 

lip,  Dorsalis  penis  sen  clitoriilis. 

13,  Muscular  brauch  to  transversus  jjerinaii. 
13',  Muscular  branch  to  erector  penis. 

13",  Muscular  branch  to  compressor  urethras. 
13'",  Muscular  branch  to  accelerator  urinoe. 
13"",  Branch  to  the  Inilb. 

asp,  Anterior  superficial  perineal  to  perineum  and  scrotum,  or  external  laliiuni. 
psp,  Posterior  superficial  perineal  to  perineum  and  scrotum,  or  external  Uil>ium. 
I  H,  Inferior  hemorrhoidal. 
IVS,  Fourth  sacral  nerve. 

14,  Muscular  branch  to  levator  ani. 
14',  Muscular  branch  to  sphincter  ani. 
14",  Muscular  branch  to  coccygeus. 

Great  sciatic  nerve. 

hj,  Branch  to  hip-joint. 

4,  Muscular  branches  to  semi-teudinosus. 
4',  Muscular  branches  to  semi-membranosus 

5,  Muscular  branches  to  adductor  magnus. 
5',  Muscular  branches  to  biceps. 

IP,   Internal  popliteal. 

0,  Muscular  branch  to  gastrocnemius  (inner  head). 
6',  Muscular  branch  to  gastrocnemius  (outer  head). 
(V,  IMuscular  branch  to  popliteus. 
6'",  Muscular  branch  to  soleus. 
PT,  Posterior  tibial  nerve. 

7,  Muscular  branch  to  tibialis  posticus. 

7',  Muscular  Ijranch  to  flexor  longus  digitorum. 

7",  Muscular  branch  to  flexor  longus  pollicis. 

pc,  Plantar  cutaneous. 

Int.  P.,  Internal  plantar  nerve. 

8,  Muscular  branch  to  abductor  pollicis. 

8',  Muscular  branch  to  flexor  brevis  pollicis. 
8",  Muscular  branch  to  first  lumbricalis. 
8'",  Muscular  branch  to  second  lumbricalis. 
8X,  Muscular  branch  to  flexor  brevis  digitorum. 
tl  to  t'i.  Digital  branches. 
Ext.  P.  External  plantar. 

li  and  (.5,  Digital  branch  to  fifth  and  outer  half  of  fourth  toe. 
10',  Muscular  branch  to  flexor  accessorius  muscle. 
10",  Muscular  branch  to  abductor  minimi  digiti. 

9,  Mu.soular  branch  to  flexor  minimi  digiti. 
9',  JIuscular  branch  to  fourth  lumbricalis. 

DB,  Deep  branch  of  external  plantar  nerve. 

9",  Deep  branch  of  external  transversalis  pedis. 
9'",  Deep  branch  of  external  third  lumbricalis. 

2>S,p2,pl,  Deep  branch  of  external  third,  second,  and  first  plantar  intcrossei  muscles. 
d4,  d3,  d-2,  dl,  Deep  branch  of  external  fourth,  third,  second,  and  first  dorsal  interossei 
muscles. 

10,  Deep  branch  of  external  adductor  pollicis. 
ES,  External  or  short  saphenous  to  outer  side  of  foot 


408  ATROPHIC    PARALYSES. 

EP,  External  popliteal. 

CP,  Communicaus  peronei. 

C,  Cutaneous  to  outer  side  of  leg. 

MC,  Musculo-cutaneous  uerve. 

11,  Muscular  branch  to  peroneus  lougus. 

11',  Muscular  branch  to  peroneus  brevis. 
AT,  Anterior  tibial  nerve. 

11",  Muscular  branch  to  tibialis  anticus 

11'",  Muscular  branch  to  extensor  lon^us  digitoruni. 

11"",  Muscular  branch  to  extensor  longus  pollicis. 

IIX,  Muscular  branch  to  extensor  brevis  digitoruni. 

Kj,  Muscular  branch  to  knee-joint. 

at,  Articxilar  branch  to  tarsus. 

Symptoms. — The  power  of  rotating  the  leg  botli  inwards  and  out- 
wards is  interfered  with,  and  that  of  abduction  is  impaired.  Some 
uncertainty  is  felt  in  standing :  the  patient  experieni-es  great  difficulty 
in  ascending  stairs,  and  when  the  body  is  inclined  forwards  it  is  difficult 
to  raise  it  to  the  erect  posture.  The  characteristic  rotation  of  the  pelvis, 
produced  by  the  contraction  of  the  gluteus  niedius  during  locomotion 
is  not  effected,  and  the  muscle  is  not  felt  rigid  on  the  side  of  the  active 
leg,  as  in  health,  when  the  hand  is  laid  over  the  pelvis  above  the 
trochanter.  Disorders  of  sensibility  are  only  present  when  other  nerves 
are  coincidentlv  affected. 


11.  Paralysis  of  the  Musclks  Sii'I'ijed  nv  the  Sackal  Plexis. 

Etiology. — Paralysis  of  the  sciatic  nerve  or  of  one  of  its  branches 
may  be  caused  by  injuries  of  various  kinds,  and  compression  of  the 
nerve  by  tumors ;  by  injury  of  the  plexus  during  the  extraction  of  the 
child  by  means  of  the  forceps,  tumors  and  abscesses  on  the  pelvis,  or 
compression  of  the  gravid  uterus,  and  by  fractures  of  the  vertebral 
column  and  tumors  of  the  cauda  equina.  Paralysis  of  the  nerve  may 
also  be  caused  by  a  rheumatic  inflammation  of  its  sheath,  and  by  neuritis 
from  extension  of  inflammation  to  it  from  neighboring  diseased  textures, 
while  it  sometimes  occurs  after  acute  diseases  and  as  a  symptom  of 
hysteria.  Paralysis  in  the  region  of  distribution  of  this  nerve  is  an 
almost  constant  symptom  of  disease  of  the  spinal  cord,  and  of  many  cases 
of  cerebral  paralysis. 

a.  In  partdysis  of  the  vmsculo-cutaneous  and  anterior  tihial  nerve i< 
(Fig.  135,  MC  and  AT)  the  foot  cannot  be  flexed  or  abducted,  and  can 
only  be  incompletely  adducted.  It  hangs  down  in  a  flaccid  condition, 
and  in  walking  the  toes,  being  depressed,  are  apt  to  trip  the  patient  at 
every  inequality  of  the  ground.  The  necessary  elevation  is  given  to 
the  foot  in  advancing  during  locomotion  by  flexion  of  the  limb  at  the 
hip-  and  knee-joints,  and  the  point  of  the  foot  is  the  last  part  to  leave 


SIMPLE    NEURAL    PARALYSES.  40!) 

tlie  grouiul  and  on  planting  it  doAvn  the  outer  border  of  the  foot  and 
the  toes  touch  the  ground  first.  This  mode  of  progression  is  frequently 
observed  in  cases  of  infantile  paralysis,  and  is  very  characteristic. 

(1)  In  parah/sis  of  the  tibialis  anticus  the  power  of  producino-  dorsal 
fiexion  and  adduction  of  the  foot  is  limited,  and  the  inner  border  and 
the  point  of  the  foot  can  no  longer  be  raised,  though  these  movements 
may  in  part  be  vicariously  executed  by  the  extensor  digitorum  communis 
and  the  extensor  longus  pollicis. 

(2)  In  paralysis  of  the  extensor  digitorum  communis  the  power  of 
producing  dorsal  flexion  of  the  foot,  and  abduction  of  it  in  the  flexed 
position  is  diminished,  and  extension  of  the  basal  phalanges  of  all  the 
toes  cannot  be  effected. 

(3)  In  paralysis  of  the  extensor  longus  -pollicis  the  power  of  pro- 
ducing dorsal  flexion  is  diminished  and  that  of  extendino-  the  great  toe 
abolished. 

(4)  In  paralysis  of  the  peroneus  longus  abduction  of  the  foot  in  the 
extended  position  is  impossible,  the  arch  of  the  foot  becomes  flattened, 
and  the  inner  border  no  longer  touches  the  ground  because  the  head  of 
the  first  metatarsal  bone  is  no  longer  drawn  downwards,  and  a  peculiar 
kind  of  flat  foot  is  thus  produced. 

(5)  In  paralysis  of  the  peroneus  hrevis  pure  abduction  of  the  foot  is 
rendered  impossible,  although  it  may  be  effected  along  with  dorsal  flexion 
by  means  of  the  extensor  digitorum  communis  and  along  with  plantar 
flexion  by  means  of  the  peroneus  longus. 

(6)  In  paralysis  of  the  extensor  digitorum  communis  hrevis  the  power 
of  extending  the  basal  phalanges  of  the  last  four  toes  is  impaired.  These 
forms  of  paralysis  may  be  combined  in  various  ways  and  then  the  affected 
muscles  can  only  be  recognized  by  the  most  careful  and  prolonged  ni- 
vestigation. 

The  sensory  disturbances  are  limited  to  the  anterior  and  external 
part  of  the  leg,  the  dorsum  of  the  foot,  and  the  greater  part  of  the  toes 
(Fig.  136,  MCS). 

h.  In  paralysis  of  the  tibial  nerve  the  patient  is  unable  to  extend  the 
foot,  or  produce  flexion  or  lateral  movements  of  the  toes. 

(1)  In  paralysis  of  the  gastrocnemius  and  soleus  the  foot  cannot  be 
extended  and  the  patient  cannot  stand  upon  the  toes,  and  when  secondary 
contraction  of  the  anterior  muscles  of  the  leg  ensues  the  foot  assumes 
a  hook-like  position  in  which  the  heel  alone  touches  the  ground,  forming 
talipes  calcaneus. 

(2)  In  paralysis  of  the  tibialis  posticus  the  power  of  abducting  the 
foot  and  of  raisinjr  its  inner  border  is  diminished. 


410 


ATEOPHIC    PARALYSES. 
Fig.  136. 


i-.^^r^ 


iL'  .A 


Cutaneous  Nerves  of  the  Lower  Extremity,    (.\fter  Flower. 

Lumbar  Plexus 

IH,  Ilio-hypogastric  uerve. 

II,  Iliu-inguiual. 

IIL,  Second  lumbar  nerve. 

GC,  Geuito-Crural. 

EC,  External  cutaneous. 

31C,  Middle  cutaneous. 

IC,  Internal  cutaneous. 

IS,  Internal  saphenous. 

PP,  Plexus  patellie. 
Sacral  Plexus. 

DP,  Dorsalis  penis  of  pudic. 

IP,  Inferior  hemorrhoidal  of  pudic. 

P,  Superficial  perineal  of  pudic  and  inferior  pudendal  nf  small  sciatic. 

IG,  Inferior  gluteal  of  small  sciatic. 

SS,  Small  sciatic. 

EP,  Branches  from  external  popliteal. 

ES,  External  saphenous. 

MCS,  Musculo-cutaneous. 

AT,  Branches  of  anterior  tibial. 

PT,  Branch  of  posterior  tibial. 


SIMPLE    XEURAL    PARALYSES.  411 

(o)  In  paralijsis  of  the  flexor  communis  digitorwn  flexion  of  the  two 
distal  phalanges  of  the  toes  is  impossible. 

(4)  In  paralysis  of  the  flexor  loncjus  polUck  flexion  of  the  great  toe 
is  incomplete. 

(."))  In  paralysis  of  the  abductor  and  adductor  poUicis  the  power  of 
moving  the  great  toe  laterally  is  lost. 

(6)  In  paralysis  of  interossei  the  patient  is  unable  to  flex  the  first  or 
to  extend  the  two  distal  phalanges  of  the  toes,  or  to  effect  separation  of 
them.  The  first  phalanges  become  hyperextended  on  the  metatarsal 
bones  and  the  distal  phalanges  are  strongly  flexed,  so  that  the  toes  no 
longer  touch  the  ground  with  their  bulbous  extremities,  and  a  claw-like 
position  is  thus  produced,  as  occurs  in  the  hand  from  paralysis  of  the 
corresponding  muscles. 

The  sensory  disorders  are  limited  to  the  posterior  surface  of  the  leg, 
the  sole  of  the  foot,  and  the  plantar  surface  of  the  toes  (Fig.  136,  PT). 

c.  In  paralysis  of  the  trunk  of  the  sciatic  nerve  all  the  muscles  of 
the  leg  and  foot  are  paralyzed,  and,  in  addition,  the  patient  is  unable  to 
flex  the  leg  upon  the  thigh,  to  approximate  the  heel  to  the  gluteal 
region,  or  to  offer  any  resistance  when  an  attempt  is  made  to  extend 
the  leg. 

The  region  of  the  knee,  the  back  part  of  the  thigh,  and  ultimately 
the  buttock  and  perineum  are  successively  affected  by  anaesthesia,  ac- 
cordincr  as  the  lesion  is  situated  at  hio-her  levels  in  the  trunk  of  the 
nerve.  If  the  lesion  is  situated  in  the  hollow  of  the  sacrum  or  in  the 
Cauda  equina  the  anaesthesia  affects  the  whole  sacral  region,  the  scrotum 
or  labia,  and  penis,  urethra,  bladder,  and  rectum. 

The  vaso-motor  disturbances  consist  of  cyanosis,  mottling  and  cold- 
ness of  the  skin  of  the  paralyzed  leg.  Increase  of  temperature  has 
occasionally  been  observed  as  a  transitory  symptom. 

The  trophic  disturbances  are  muscular  atrophy,  ulceration  of  the 
skin,  eruptions  of  herpes  and  pemphigus,  and  liedsores  on  the  sacrum, 
ankles,  and  heels. 


CHAPTER    YI. 

ATROPHIC  PARALYSES  {continued). 
II.  MULTIPLE   NEURAL   PARALYSES. 

1.  Idiopathic  PiiOdREssivio  Mri/rii>i,i-;  Nkuritis. 

This  affection  is  usually  ushered  in  by  more  or  less  fever  ;  the  patient 
soon  complains  either  simultaneously  or  successively  of  tingling  pains 
and  feelings  of  coldness  and  numbness  in  the  feet  and  hands,  the  terri- 
tory  of  the  ulnar  nerve  being  peculiarly  liable  to  be  affected  at  an  early 
period  of  the  disease.  Pressure  over  circumscribed  spots  of  the  nerves 
causes  great  pain,  which  radiates  towards  tlie  periphery,  and  both  the 
skin  and  the  muscles  in  the  area  of  distribution  of  the  affected  nerves 
are  so  extremely  sensitive  to  pressure  that  the  patient  avoids  any  move- 
ment of  the  limbs,  and  complains  bitterly  of  the  slightest  touch  or  of 
passive  movements.  Alongside  this  hypencsthesia  to  pressure  there  is 
well-marked  anjesthesia  of  certain  forms  of  sensibility.  Tactile  sensi- 
bility is  indistinct,  and  the  patient  is  unable  to  localize  accurately,  with 
closed  eyes,  a  point  touching  the  skin,  or  to  distinguish  two  points  as 
separate  until  they  are  far  removed  from  one  another.  In  the  early 
stage  of  the  disease  it  is  somewhat  difficult  to  distinguish  whether  the 
motionless  condition  of  the  limbs  arises  from  the  reluctance  of  the 
l)atient  to  move  them  for  fear  of  provoking  pain,  or  from  decided 
motor  paralysis.  Soon,  however,  distinct  paralysis  sets  in,  and  the 
affected  muscles  undergo  rai)id  atrophy  and  manifest  the  ''  reaction  of 
degeneration."  The  paralysis  begins  in  the  small  muscles  of  the  hands 
and  feet,  gradually  spreads  upwards,  and  successively  invades  the  larger 
muscles  of  the  limbs  and  those  of  the  trunk,  while  in  some  cases  the 
muscles  of  the  bladder  and  rectum  are  involved.  The  small  muscles  of 
the  hands  and  the  extensors  of  the  forearm  are  usually  affected  to  a 
greater  degree  than  the  other  muscles  of  the  upper  extremities,  and, 
consequently,  the  fingers  and  hands  assume  distorted  positions  similar 
to  the  claw-hand  of  progressive  muscular  atrophy.  Some  of  the  cutaneous 
reflexes  may  be  normal,  while  others  are  variously  altered.  The  plantar 
reflex  is  absent  in  the  advanced  stage  of  the  disease ;  even  at  first  it  is 
absent  to  slight  stimulation,  but  a  strong  stimulus  is  said  to  provoke  an 


MULTIPLE    NEURAL    PARALYSES.  413 

exaggerated  reaction.  The  tendon-reactions,  and  more  especially  the 
patellar  tendon-reaction,  appear  to  be  abolished  at  an  early  period  of 
the  disease.  The  affected  nerves  are,  as  already  mentioned,  painful  on 
pressure  of  particular  ])oints,  and  at  times  the  nerve  may  be  felt  to  be 
distinctly  swollen  at  these  points ;  while  in  some  cases  it  may  be  the 
seat  of  an  oedematous  swelling  of  considerable  size.  The  trophic  dis- 
orders consist,  besides  the  atrophy  of  the  muscles  already  described,  of 
alterations  of  the  nails,  which  sometimes  become  brittle,  cracked, 
strongly  curved,  and  of  a  yellowish  or  brownish  color  :  and  of  an  in- 
creased develojunent  of  hair,  or  in  some  cases  disappearance  of  the  hair 
from  some  spots  of  the  skin,  the  skin  of  the  fingers  being  especially 
liable  to  become  hairless  and  glossy.  Patches  of  the  skin  are  liable  to 
become  of  a  red  or  bluish  color  from  vaso-motor  changes,  and  the  sub- 
cutaneous tissue  may  also  become  decidedly  a?dematous. 

In  its  onset  progressive  multiple  neuritis  is  essentially  an  acute  affec- 
tion, considerable  sensory  and  motor  disturbances  beincr  established  in 
the  course  of  a  few  days.  In  its  further  progress  the  affection  becomes 
chronic,  and  any  change  which  takes  place  either  by  way  of  amend- 
ment or  extension  of  the  disease  may  occupy  many  weeks.  After  from 
nine  to  eighteen  months,  complete  recovery  may  take  place  or  the 
recovery  may  be  partial,  the  muscles  supplied  by  the  ulnar  nerve  re- 
maining sometimes  permanently  disabled.  The  disease  sometimes  termi- 
nates fatally  from  implication  of  the  intercostal  and  bulbar  nerves,  but 
the  fatal  result  is  often  caused  by  a  complication  like  chronic  nephritis, 
or  an  intercurrent  affection  like  pneumonia  or  tiiberculosis. 

2.  Leau  Paralysis. 

Almost  all  the  muscles  of  the  body  may  be  affected  by  an  atrophic 
paralysis  in  chronic  lead-poisoning,  although  certain  groups  are  attacked 
by  preference.  In  partial  paralysis  the  extensor  muscles  of  the  fore- 
aiTii  are  more  frequently  affected  than  any  other  group,  and  consequently, 
Avhen  the  arms  are  held  out  horizontally,  with  the  hands  in  a  state  of 
pronation  the  hands  hang  powerless,  this  condition  being  graphically 
called  ivrist-drop.  The  common  extensors  of  the  fingers  are  the  first 
to  be  attacked,  then  the  extensors  of  the  index  and  little  fingers,  the 
extensor  secundii  internodii  pollicis,  the  extensors  of  the  wrist,  the 
extensor  primi  internodii  pollicis,  and  the  extensor  ossis  metacarpi  pollicis 
are  successively  invaded.  The  supinator  longus  is  spared  until  a  com- 
paratively late  period  of  the  disease  and  it  is  never  invaded  unless  the 
paralysis  extend  to  the  muscles  of  the  upper  arm.  Occasionally  the 
paralysis  may  begin   in   the  muscles  of  the  upper  arm  and  then  the 


41-i  ATROPHIC    PARALYSES, 


deltoid,  biceps,  brachialis  anticus,  and  supinator  longus  are  almost  simul- 
taneously attacked.  When  the  muscles  of  the  inferior  extremities  are 
paralyzed,  the  anterior  muscles  of  the  leg  are  generally  the  first  to  be 
attacked,  and  the  extensor  muscles  of  the  thigh  are  the  next  most 
likely  to  be  invaded.  In  some  cases  all  the  muscles  of  both  upper  and 
lower  extremities  are  paralyzed,  whilst  on  rare  occasions  the  muscles  of 
the  thorax  and  back,  those  of  phonation  and  speech,  the  intercostal 
muscles,  and  even  the  diaphragm  have  been  implicated.  Paralysis  of 
the  muscles  of  the  glottis  has  been  observed  by  Trousseau  in  horses 
employed  in  red  lead  factories.  The  sphincters  remain  always  unaffected 
in  the  paraplegic  form.  The  paralyzed  muscles  undergo  rapid  atrophy, 
and  lose  their  faradic  contractility  before  voluntary  power  is  completely 
abolished,  while  the  galvanic  degeneration  reaction  appears  in  them  at 
an  early  period.  The  patellar  tendon-reaction  is  often  lost  in  cases  in 
which  there  is  no  perceptible  atrophy  of  the  muscles  of  the  lower  ex- 
tremities, but  I  have  found  this  reaction  present  in  several  cases  in 
which  the  wrist-drop  was  very  pronounced. 

Tremor  is  sometimes  observed  in  lead-poisoning ;  it  is  often  limited  to 
the  upper  extremities,  but  may  become  general  in  aggravated  cases. 
Ataxic  symptoms  have  occasionally  been  observed  along  with  anaesthesia. 

Sensory  disorders  are  often  absent  in  cases  of  wrist-drop,  but  when 
the  paralysis  extends  to  the  muscles  of  the  lower  extremities  a  good 
deal  of  anaesthesia  may  be  present,  especially  in  the  area  of  distribution 
of  the  cutaneous  branches  of  the  external  popliteal  nerve.  In  some 
cases,  however,  the  skin  over  the  back  of  the  hands  and  forearms  is 
more  or  less  aniesthetic,  and  a  certain  degree  of  loss  of  feeling  may  Ije 
observed  over  the  surface  of  the  chest  and  abdomen,  whilst  in  a  few 
cases  the  veil  of  the  palate  and  uvula,  and  even  the  conjunctiva,  may  be 
completely  ansesthetic.  Symptoms  of  sensory  irritation  are  also  often 
present  in  chronic  lead-poisoning.  Cutaneous  hypertvsthesia  may 
accompany  attacks  of  pain,  while  drthralgia,  occurring  in  paroxysms 
and  situated  either  in  the  extremities  or  in  the  jaws,  is  often  a  promi- 
nent symptom. 

Lead  colic  is  one  of  the  most  frequent  and  important  symptoms  of 
the  disease ;  the  pains,  which  are  chiefly  referred  to  the  umbilical  region, 
are  more  or  less  continuous,  but  they  are  liable  to  paroxysmal  exacerba- 
tions of  great  severity.  The  special  senses  are  sometimes  aflfected. 
Diminution  of  taste  on  one-half  the  tongue  and  of  smell  in  one  nostril 
has  been  observed,  but  deafness  is  said  to  result  only  from  local  disease 
of  the  ear.  But  visual  disorders  are  more  frequent  and  more  important 
than  those  of  the  other  special  senses.  These  consist  of  transitory 
amblyopia   without    ophthalmoscopic    changes;    persistent    amblyopia 


MULTIPLE    NEURAL    PARALYSES.  415 

passing  on  to  amaurosis  of  both  eyes  and  rarely  of  one  only,  attended 
by  atrophy  of  the  optic  nerve :  amblyopia  with  double  optic  neuritis, 
and  amblyopia  with  albuminuric  retinitis  in  association  with  oranular 
kidneys. 

Psychical  disorders  are  often  present  in  aggravated  cases.  Before 
the  outbreak  of  pronounced  cerebral  symptoms  the  patient  generallv 
suffers  from  headache,  vertigo,  and  drowsiness  during  the  day  with 
sleeplessness  at  night ;  or  there  may  be  a  state  of  agitation,  or  complete 
apathy.  The  psychical  disorders  consist  of  hallucinations  of  sight  and 
hearing,  with  a  quiet  delirium,  or  the  patient  may  have  an  attack  of 
furious  delirium.  Convulsions  are  frequently  present,  and  they  may  be 
partial,  being  then  limited  to  the  muscles  of  the  face  or  to  one  or  more 
of  the  hmbs,  or  they  may  assume  the  form  of  an  attack  of  eclampsia. 
These  convulsions  are  generally  followed  by  a  stage  of  profound  un- 
consciousness with  stertorous  breathing.  Apoplectiform  attacks  are 
liable  to  occur  in  the  last  stage  of  lead  paralysis,  and  inasmuch  as  the 
patient  often  recovers  motor  power  quickly  these  attacks  cannot  always 
be  due  to  hemorrha£:e. 


3.  Alcoholic  Paralysis. 

Persons  who  have  indulged  too  freely  in  the  use  of  alcohol  are  liable 
to  suffer  fi'om  a  progressive  paralysis  which  is  accompanied  by  more 
or  less  rapid  atrophy  of  the  affected  muscles.  The  affection  generally 
begins,  so  far  as  the  paralysis  is  concerned,  by  a  gradually  increasing 
weakness  of  the  lower  extremities.  The  patient,  after  suffering  from 
numbness,  tearing  pains,  and  often  also  from  distressing  cramps  in  the 
lower  extremities,  experiences  a  progressively  increasing  difficulty  in 
maintaining  the  erect  posture,  and  on  attempting  to  walk  the  legs  are 
spread  asunder  in  order  to  widen  the  base,  while  the  gait  is  uncertain, 
or  walking  may  be  impossible  Avithout  the  support  of  tAvo  sticks  or  of 
an  attendant.  The  movements  of  the  hands  are  also  sometimes  irregu- 
lar and  uncertain  and  when  an  arm  is  stretched  out  to  perform  an  in- 
tended movement  the  object  may  only  be  reached  after  numerous  slight 
lateral  and  vertical  jerking  interruptions.  At  this  stage  of  the  disease 
the  alcoholic  subject,  provided  the  person  be  sober  during  examination, 
appears  to  be  in  a  moderately  advanced  stage  of  locomotor  ataxia,  and 
the  similarity  between  the  two  diseases  is  rendered  still  more  striking 
by  the  fact  that  the  patellar  tendon-reaction  is  absent  in  the  alcoholic 
disease  as  well  as  in  ataxia.  A  closer  examination,  however,  will  show 
that  the  alcoholic  affection  is,  from  the  first,  a  paralytic  one.  Provided 
the  patient  is  able  to  walk,  it  Avill  be  seen  that  the  toe  of  the  advancing 


4:16  ATEOPHIC    PARALYSES. 

foot  ahvays  drops,  just  as  occurs  in  cases  of  infantile  paralysis  ^vllen  the 
extensors  of  the  foot  and  toes  are  paralyzed,  and  when  the  legs  of  the 
patient  are  uncovered  in  bed  it  will  be  seen  that  the  feet  assume  the 
position  of  paralytic  talipes  equinus.  or  rather  talipes  equina  varus, 
because  the  tibialis  anticus  is  not  paralyzed  to  the  same  degree  as  the 
extensors  and  peronei  muscles.  It  will  also  be  found  that  the  extensors 
of  the  front  of  the  thigh  are  very  feeble.  A  methodical  examination  of 
the  upper  extremities  proves  equally  instructive.  The  patient  on  holding 
his  arms  out  horizontally,  the  forearms  being  in  a  state  of  pronation,  may 
be  able  to  hold  the  hands  and  fingers  extended,  Init  the  slightest  pres- 
sure on  the  backs  of  the  fingers  causes  flexion  at  the  metacarpo-phalan- 
geal  joints,  on  the  back  of  the  hand  causes  flexion  at  the  wrist,  and  in 
many  cases  the  little  finger  is  seen  to  drop,  the  patient  being  unable  to 
maintain  it  fully  extended  at  the  metacarpo-phalangeal  joint.  On 
electrical  exploration  the  faradic  contractility  will  ]je  ascertained  to  be 
much  diminished  or  completely  lost  in  the  extensors  of  the  leg  and 
those  of  the  front  of  the  thigh,  and  considerably  diminished  in  the 
extensors  of  the  forearm,  while  the  galvanic  excitability  of  these  mus- 
cles manifests  the  qualitative  changes  of  the  "  reaction  of  degeneration."' 

After  another  deep  carouse  the  whole  clinical  picture  of  the  disease 
changes.  The  patient  now  lies  helpless  in  bed,  being  unable  to  stand, 
and  possibly  not  even  to  sit  up  in  bed.  But  the  most  remarkable 
feature  of  this  stage  of  the  disease  is  presented  by  the  upper  extremi- 
ties. The  extensors  of  the  forearms  are  completely  paralyzed  and  a 
double  wrist-drop  results  just  as  in  lead  paralysis,  and  to  render  the 
similarity  between  the  two  diseases  more  striking  the  supinator  longiis 
is  comparatively  spared  in  the  former  as  in  the  latter  disease.  The 
flexors  of  the  fingers  and  wrist  and  the  intrinsic  muscles  of  the  hand 
are  also  very  feeble,  but  I  have  not  seen  them  completely  paralyzed. 
In  the  upper  arm  the  triceps  is  much  more  feeble  than  the  biceps,  and 
consequently  the  forearm  is  maintained  during  repose  at  a  right  angle 
to  the  arm,  but  when  the  patient  moves  the  extremity  the  forearm  becomes 
flexed  at  an  acute  angle  to  the  arm,  and  the  curled-up  attitude  now 
assumed  by  the  extremity  may  appear  to  a  superficial  observer  to  be 
imposed  upon  it  by  an  active  spasm  and  not  by  a  paralysis,  so  that  the 
disease  has  a  certain  resemblance  to  tetany.  The  movements  at  the 
shoulder  are  not  much  interfered  with.  On  electrical  exploration  it  will 
now  be  found  that,  speaking  generally,  the  extensors  of  both  lower  and 
upper  extremities  give  the  complete,  and  the  remaining  muscles  of  the 
limbs  Erb's  partial,  "reaction  of  degeneration." 

If  the  disease  advances  further,  the  diaphragm  becomes  paralyzed 
and  the  abdomen  sinks  as  the  chest  expands  and  protrudes  slightly  as 


ML'LTIPLE    NEURAL    PARALYSES.  417 

the  chest  contracts.  At  a  still  later  period  the  intercostal  muscles 
become  paralyzed,  and  the  patient  after  a  short  interval,  in  which  the 
breathing  is  maintained  by  the  upper  thoracic  muscles,  dies  from 
asphyxia.  The  order  in  Avhich  the  various  muscular  groups  are 
attacked  is  important,  because  in  all  the  ascending  forms  of  spinal 
paralysis  the  intercostal  muscles  are  affected  before  the  diaphragm,  and 
the  intrinsic  muscles  of  the  hand  before  the  extensors  of  the  forearm. 
The  cutaneous  reflexes  and  the  mechanical  irritability  of  the  affected 
muscles  are  diminished  or  absent,  Avhile  the  tendon  reactions  are  nearly 
always  lost  at  an  early  period  of  the  disease. 

Sensory  disturbances  are  always  present.  The  patients  suffer  from 
tearing  pains  in  the  lower  extremities  which  are  apt  to  become  pecu- 
liai'ly  distressing  at  night,  and  they  complain  of  a  distressing  burning 
of  the  feet,  as  well  as  of  numbness  and  various  other  parjesthesite. 
Cutaneous  hypersesthesia  is  occasionally  present,  but  it  is  by  no  means 
in  so  marked  a  degree  as  muscular  hypersesthesia,  which  forms  one  of 
the  most  characteristic  features  of  the  disease.  The  slightest  pressure 
on  the  muscle  calls  forth  loud  cries  from  the  patient,  and  suffices  to 
induce  in  females  a  prolonged  attack  of  hysterical  sobbing.  The 
hvpersesthesia  of  the  lower  extremities,  most  probably  that  of  the  mus- 
cles, is  indeed  sometimes  so  great  that  the  weight  of  the  bedclothes  is 
intolerable  to  the  patient,  and  the  feet  have  to  be  protected  by  cradles. 
The  sense  of  temperature  is  sometimes  perverted  in  such  a  way  that  all 
objects  feel  cold  on  contact.  In  the  more  advanced  stages  of  the  dis- 
ease, the  hypertBsthesia  gives  place  to  more  or  less  ansesthesia,  sensory 
conduction  is  retarded,  the  tactile  sense  is  diminished,  and  Remak's 
double  sensation  may  be  observed.  At  times,  the  spine  is  tender  to 
pressure,  but  pain  and  stiffness  of  the  vertebral  column  are  not  promi- 
nent symptoms. 

Vaso-motor  disorders  are  generally  present  in  the  form  of  redness  of 
the  feet,  and  of  oedema  of  the  ankles  and  backs  of  the  feet  and  hands. 
The  oedema  of  the  lower  extremities  is  sometimes  present  to  so  great  a 
degree  as  to  suggest  the  presence  of  a  cardiac  complication,  but  a 
physical  examination  negatives  this  idea. 

The  trophic  disorders  consist  of  local  asphyxia,  and  even  gangrene 
of  the  extremities  has  been  occasionally  observed  as  a  complication. 
Psychical  disturbances  are  by  no  means  rare  ;  they  consist  of  restless- 
ness, sleeplessness,  marked  loss  of  memory  with  diminished  intelligence 
and  a  stupid  and  stolid  expression,  delusions  or  hallucinations,  and 
delirium,  these  being  present  either  separately  or  in  various  combnia- 
tions.  The  girdle  sensations,  disorders  of  the  movements  of  the  pupils 
and  eyeballs,  disturbances  of  the  functions  of  the  bladder  and  rectum, 

27 


418  ATROPHIC    PARALYriES. 

and  arthropathies,  which  are  so  frequently  observed  and  so  characteristic 
of  tabes  dorsalis,  are  absent  in  alcoholic  paralysis. 

Alcoholic  paralysis  is  said  to  occur  Avith  greater  frequency  in  women 
than  in  men,  but  without  questioning  the  truth  of  this  statement,  I  am 
convinced  that  it  is  more  frequent  in  men  than  is  generally  supposed. 
Out  of  eight  well-marked  cases  of  the  disease  which  I  have  seen  within 
the  last  six  months,  four  were  men  and  four  women,  and  of  these,  two 
men  and  two  women  had  complete  double  wrist-drop.  One  man  died 
from  respiratory  paralysis  and  a  woman  from  cerebral  complication  ;  of 
the  remaining  six",  one  has  almost  completely  recovered  and  five  are  still 
under  treatment. 

The  symptoms  of  the  pronounced  form  of  alcoholic  paralysis  in  which 
double  wrist-drop  occurs  begin  more  or  less  acutely,  generally  after  an 
unusually  deep  carouse,  but  as  a  rule  the  affection  assumes  a  chronic 
course,  although  a  few  cases  are  rapidly  fatal  from  respiratory  paralysis. 
In  chronic  cases  death  may  take  place  from  a  cerebral  complication  or 
from  an  intercurrent  disease  such  as  cirrhosis  of  the  liver.  Most  cases, 
however,  recover  completely,  provided  the  use  of  alcohol  is  wholly  pro- 
hibited, but  a  relapse  is  liable  to  take  place  on  recurrence  to  the  old 
habit,  and  when  through  long  indulgence  the  affection  becomes  very 
chronic,  the  paralysis  may  prove  incurable. 

4.  DiPHTTiKRiTic  Paralysis. 

Diphtheritic  paralysis  begins  occasionally  towards  the  close  of  the 
febrile  attack,  but  in  most  cases  it  does  not  declare  itself  until  from  eight 
days  to  three  weeks  or  more  after  the  disappearance  of  the  false  mem- 
brane from  the  throat.  The  first  symptom  to  attract  attention  is  a  nasal 
quality  of  voice  and  the  ejection  of  fluids  through  tlie  nose,  caused  by 
paralysis  of  the  veil  of  the  palate,  and  when  the  back  of  the  throat  is 
examined  it  is  seen  that  the  soft  palate  hangs  loose  and  flap])ing  from 
the  roof  of  the  mouth,  and  that  it  is  not  retracted  on  reflex  irritation 
or  during  phonation,  deep  inspiration,  and  attempts  at  deglutition.  The 
patient  can  swallow  solids  better  than  fluids,  inasmuch  as  the  latter  are 
more  readily  ejected  through  the  nose  than  the  former,  but  when  the 
pharyngeal  muscles  become  paralyzed,  as  they  frequently  do,  the  diffi- 
culty of  deglutition  becomes  greater,  and  the  patient  is  in  danger  of 
being  starved  from  inability  to  swallow  sufficient  food,  or  of  being  suf- 
focated by  the  bolus  becoming  impacted  in  the  pharynx,  or  finding  its 
way  into  the  air-passages,  the  latter  accident  being  much  facilitated  by 
the  fact  that  anaesthesia  of  the  mucous  membrane  of  the  superior  part 
of  the  larynx  is  often  superadded  to  the  palatal  and  pharyngeal  paralysis. 


MULTIPLE    XEUKAL    PARALYSES.  419 

Difficulty  of  respiration  may  be  caused  by  paralysis  of  the  abductors  of 
the  vocal  cords,  or  the  voice  may  be  altered  from  a  slight  deo^ree  of 
hoarseness  up  to  complete  aphonia,  owing  to  paralysis  of  the  muscles 
which  render  tense  and  approximate  the  vocal  cords.  The  tongue,  the 
lips,  and  the  masticatory  muscles  may  likewise  be  more  or  less  paralyzed, 
and  the  symptoms  then  are  very  like  those  of  progressive  bulbar  paralysis. 
But  the  ocular  muscles,  and  especially  the  internal  muscles  of  the  eye 
are  those  which  are  most  frequently  attacked  after  the  muscles  of  the 
throat.  The  patient  is  unable  to  read  small  print  and  cannot  accom- 
modate the  eye  for  near  objects,  this  defect  being  due  to  paralysis  of 
the  ciliary  muscle,  and  mydriasis  has  occasionally  been  observed  from 
paralysis  of  the  sphincter  of  the  iris.  Paralysis  of  one  or  more  of  the 
external  muscles  of  the  eye  is  declared  by  the  presence  of  diplopia  or 
strabismus,  while  ptosis  on  one  or  both  sides  reveals  paralysis  of  the 
elevator  muscle  of  the  eyelid.  Complete  paralysis  of  the  facial  muscles 
has  not  been  observed  in  diphtheritic  paralysis,  but  a  certain  degree  of 
immobility  of  the  face  is  often  present,  which,  when  conjoined  to  the 
defect  of  vision,  gives  to  the  patient  an  idiotic  expression,  although 
psychical  disturbances  are  absent  during  the  whole  course  of  the  disease, 
except  perhaps  some  degree  of  apathy  and  a  disinclination  to  make  any 
intellectual  effort.  The  paralysis  now  extends  to  the  muscles  of  the 
limbs,  and  the  inferior  extremities  are  usually  the  first  to  be  attacked, 
but  in  most  cases  the  muscles  of  the  superior  extremities  are  subsequently 
implicated,  and  ultimately  those  of  the  trunk,  including  the  muscles  of 
respiration,  may  be  invaded. 

In  most  cases  the  motor  disorder  simply  amounts  to  a  certain  degree 
of  feebleness  of  the  limbs,  which  manifests  itself  in  an  uncertain  and 
staggering  gait  that  may  be  mistaken  for  ataxia,  the  similarity  between 
the  two  aftections  being  rendered  still  closer  by  the  presence  in  diph- 
theritic paralysis  of  certain  sensory  disorders,  which  will  be  immediately 
described,  and  absence  of  the  patellar  tendon-reflex.  The  paralysis 
after  a  time  increases  in  intensity  and  extent,  and  the  feebleness  of  the 
lower  extremities  may  become  so  great  that  the  patient  is  unable  to 
maintain  the  erect  posture  and  becomes  confined  to  his  bed,  while  the 
upper  extremities  are  so  much  affected  that  the  patient  is  unable  to 
button  his  clothes,  or  to  carry  a  spoon  to  his  mouth,  and  the  difficulty 
of  seizing  small  objects  is  greatly  increased  by  the  presence  of  sensory 
disorders.  The  muscles  of  the  neck  may  be  paralyzed  even  before 
those  of  the  extremities.  After  a  time  the  erector  muscles  of  the  spine 
are  invaded,  and  the  patient  may  then  be  unable  even  to  sit  up  in  bed. 

In  some  cases  the  paralysis  assumes  the  hemiplegic  form,  but  a  care- 
ful examination  shows  that  the  side  which  is  presumed  to  be  healthy  is 


420  ATROPHIC    PARALYSES. 

enfeebled,  and  that  the  hemiplegic  distribution  of  the  paralysis  arises 
from  the  fact  that  there  is  a  disproportion  between  the  degree  to  which 
the  motor  weakness  has  attained  on  each  side  of  the  body.  The  dia- 
phragm may  ultimately  be  paralyzed,  and  should  the  intercostal  muscles 
be  simultaneously  attacked  the  danger  of  death  from  asphyxia  is  great. 

Sensory  disorders  always  accompany  the  loss  of  motor  poAver  in 
diphtheritic  paralysis.  The  mucous  membrane  of  the  soft  palate  and 
pharynx  is  anaesthetic,  and  the  tactile  sensibility  of  the  mucous  mem- 
brane of  the  lips,  cheeks,  and  tongue  is  often  diminished.  The  motor 
disorders  of  the  extremities  are  accompanied,  or  possibly  preceded,  by 
sensory  phenomena,  the  patient  complains  of  numbness  and  tingling 
pains  in  the  feet  and  hands,  and  of  a  feeling  of  cold  and  of  weight  in 
the  limbs,  the  tactile  sensibility  is  blunted,  and  in  some  cases  there  is 
complete  anesthesia.  The  inferior  extremities  are  usually  the  first  to 
be  affected,  and  patients  cannot  then  feel  the  ground  on  which  they 
tread,  or  feel  it  only  imperfectly ;  they  often  state  that  it  seems  as  if 
they  were  walking  on  cotton,  wool,  or  some  other  soft  substance,  and 
they  are  unable  to  walk  with  closed  eyes  without  danger  of  falling, 
just  as  occurs  in  locomotor  ataxia.  AVhen  the  hands  are  attacked  the 
patients  feel  as  if  their  fingers  were  covered  with  gloves,  and  tactile 
sensibility  may  be  so  blunted  that  the  person  is  unable  to  seize  and 
hold  small  objects  without  tlie  aid  of  sight.  The  disorders  of  cutane- 
ous sensibility  are  very  variable  in  their  extent  and  distribution,  as 
well  as  in  their  degree  of  intensity.  The  anaesthesia  begins  in  the 
periphery  of  the  limbs  and  extends  towards  the  trunk ;  it  often  remains 
limited  to  the  distal  segments  of  the  extremities,  but  sometimes  becomes 
general,  and  Trousseau  mentions  a  case  in  which  the  patient  had  almost 
no  consciousness  of  the  passage  of  the  urine  and  feces,  although  mic- 
turition and  defecation  Avere  voluntarily  performed.  In  a  few  cases  the 
anaesthesia  has  been  limited  to  the  superior  extremities,  and  in  excep- 
tional cases  cutaneous  hypertesthesia,  accompanied  by  articular  pains, 
has  been  observed.  The  special  senses  are  also  sometimes  affected  in 
diphtheritic  paralysis.  We  have  already  seen  that  vision  is  rendered 
indistinct  by  paralysis  of  the  ciliary  muscles,  but  in  other  cases  ambly- 
opia, proceeding  to  complete  amaurosis,  may  result  from  insensibility  of 
the  retinae.  Taste  has  occasionally  been  found  diminished,  probably 
never  abolished,  but  loss  of  smell  and  deafness  have  been  more  fre- 
quently observed. 

The  reflex  action  of  the  palate  is  diminished  or  lost  at  an  early 
period  of  the  disease,  but  there  are  not  very  accurate  statements  with 
regard  to  the  reflex  actions  of  the  extremities.  The  patellar  tendon- 
reactions  are  lost  even  before  paralysis  of  the  lower  extremities  becomes 


MULTIPLE    NEURAL    PARALYSES.  -i21 

very  pronounced  and  consequently  the  liability  to  mistake  diphtheritic 
paralysis,  at  a  certain  stage  of  its  development,  for  locomotor  ataxia  is 
very  great.  The  paralyzed  muscles  manifest  the  reaction  of  degenera- 
tion on  electrical  exploration. 

Visceral  disorders  are  numerous  and  important  in  this  form  of  paral- 
ysis. We  have  already  seen  that  the  respiratory  muscles  may  be 
attacked,  and  that  the  disease  may  terminate  fatally  by  arrest  of  res- 
piration. In  other  cases  the  heart  becomes  affected  with  paralysis. 
The  cardiac  disorder  is  manifested  by  an  excessively  slow,  irregular, 
and  feeble  pulse,  and  by  paroxysms  of  palpitation,  accompanied  by 
precordial  anxiety  and  dyspnoea.  The  nervous  disorders  are  sometimes 
ushered  in  by  a  remarkable  slowing  of  the  pulse,  attacks  of  syncope, 
and  vomiting,  all  of  these  being  symptoms  which  are  to  be  referred  to 
interference  Avith  the  functions  of  the  pneumogastric  nerve,  and  at  a 
late  period  of  the  disease  the  patient  may  suffer  from  prsecordial  agony, 
and  the  pulse  becomes  slow,  irregular,  and  so  small  as  to  be  almost 
undistinguishable,  while  death  by  syncope  is  not  uncommon.  I  have 
known  glycosuria  to  occur  after  an  attack  of  diphtheria,  and  the  patient 
has  since  made  a  complete  recovery.  Obstinate  constipation  is  a  fre- 
(juent  symptom  of  diphtheritic  paralysis  ;  it  is  usually  a  late  symptom, 
and  generally  appears  after  the  extremities  are  invaded,  but  in  the  last 
stage  of  the  disease  the  rectum  may  be  paralyzed,  and  then  constipa- 
tion is  succeeded  by  an  involuntary  discharge  of  feces.  After  a  time 
the  urinary  organs  may  become  affected ;  the  bladder  becomes  greatly 
distended,  and  unless  the  catheter  be  used,  dribbling  of  urine  occurs 
from  overdistention ;  but  this  is  succeeded  by  paralysis  of  the  sphincter, 
with  incontinence.  The  patient  likewise  loses  his  virile  power,  and  in 
some  cases  there  is  complete  impotence. 

The  duration  of  diphtheritic  paralysis  is  very  variable.  When  the 
veil  of  the  palate  alone  is  affected  the  paralysis  disappears,  as  a  rule,  in 
from  ten  days  to  three  weeks,  but  when  the  paralysis  is  widely  distributed 
over  the  body  it  lasts  from  two  to  four  months,  but  rarely  persists  beyond 
six  months.  Diphtheritic  paralysis  usually  terminates  in  complete  re- 
covery or  death,  and  only  very  exceptional  cases  are  recorded  in  which 
the  recovery  was  incomplete.  About  twelve  per  cent,  of  all  cases 
terminate  fatally,  death  taking  place  by  asphyxia  from  respiratory 
paralysis  or  from  food  getting  into  the  glottis,  inanition  from  inability 
to  swallow,  nervous  exhaustion,  or  syncope. 


422  ATEOPHIC    PARALYSES. 

III.  EEFLEX   ATPvOPHIC    PAEALYSES. 

Etiology. — The  most  characteristic  examples  of  this  form  of  atrophic 
paralysis  are  to  be  found  in  chronic  diseases  of  the  joints,  Avhilo  the 
extensor  muscles  are  often  found  to  be  feeble  and  emaciated.  It  is  a\  ell 
known  to  surgeons  that  the  deltoid  is  often  feeble  and  wasted  in  chronic 
disease  of  the  shoulder-joint,  while  Hunter  and  more  recently  Adams 
directed  attention  to  the  flattening  of  the  gluteal  region  which  is 
observed  in  chronic  disease  of  the  hip-joint.  The  extensors  of  the 
thigh  are  liable  to  become  feeble  and  emaciated  in  diseases  of  the  knee- 
joint,  and  the  extensors  of  the  fingers  and  thumb,  and  to  a  less  extent 
the  flexors  also,  are  similarly  afl'ected  in  cases  of  rheumatoid  arthritis. 
In  some  cases  a  slight  and  transitory  synovitis  gives  rise  to  a  degree  of 
paralysis  and  wasting  of  the  extensor  muscles  which  is  altogether  dis- 
proportionate to  the  severity  and  duration  of  the  joint  affection. 

The  aflection  described  under  the  name  of  reflex  or  urinary  para- 
plegia does  not  differ  in  its  causation  from  the  paralysis  of  joint 
diseases,  being  set  up  by  irritation  of  one  of  the  viscera,  such  as  the 
urinary  organs,  uterus,  or  intestinal  canal.  The  cause  of  the  paralysis 
is  sometimes  an  injury  or  neuritis  of  a  peripheral  nerve.  In  severe 
cases  of  neuritis  from  injury  the  inflammatory  process  may  pursue  an 
ascending  course  and  set  up  an  acute  or  subacute  myelitis,  but  in  the 
cases  under  consideration  at  present  it  is  probable  that  the  symptoms 
are  caused  by  irritation  of  the  gray  matter  in  the  absence  of  serious 
structural  changes. 

Symptoms. — In  paralysis  of  the  extensors  secondary  to  diseases  of 
the  joints,  the  affected  muscles  become  soft  and  flabby,  and  emaciated, 
while  their  motor  power  is  greatly  diminished.  The  mechanical  irrita- 
bility of  the  afl'ected  muscles  is  increased,  the  reaction  of  their  tendons  is 
normal  or  slightly  exaggerated,  and  lively  contractions  are  said  Ijy  Charcot 
to  be  obtained  by  passing  sparks  of  static  electricity  through  them,  but 
the  faradic  and  galvanic  excitability  is  diminished  without  qualitative 
changes.  In  cases  of  rheumatoid  arthritis  the  muscles  of  the  body  often 
undergo  a  diffused  atrophy  which  predominates  in  the  extensors.  The 
deltoid,  the  triceps,  the  extensors  of  the  wrist,  fingers,  and  thumb,  the 
gluteal  muscles,  the  extensors  of  the  thigh,  and  the  extensors  of  the  toes 
are  feeble  and  emaciated,  and  although  the  flexors  are  likewise  implicated, 
yet  the  paralysis  in  them  being  to  a  less  degree  they  undergo  adapted 
contractions  and  the  limbs  become  then  fixed  in  flexed  positions.  The 
mechanical  irritability  of  the  partially  paralyzed  muscles  is  in  excess, 
the  tendon-reactions  are  exaggerated,  and  even  ankle  clonus  may  be 
elicited  in  both  ankles. 


REFLEX  ATROPHIC  PARALYSES.  423 

111  urinary  paraplegia  the  lower  extremities  are  paretic,  but  never 
completely  paralyzed :  the  reflexes  are  said  now  to  be  increased ;  and 
there  is  complete  absence  of  pains  in  the  loins,  girdle  pains,  dys^sthesiic. 
anassthesia,  muscular  tension  and  contractures,  paralysis  of  the  bladder, 
and  bedsores  and  other  trophic  disturbances.  The  gait  corresponds  to 
the  well-known  shuffling  gait  of  old  age  and  is  never  of  the  spastic 
variety.  The  paralysis  is  very  variable  in  its  degree  and  extent  and 
rapid  improvement  may  take  i>lace  if  there  be  an  amelioration  of  the 
peripheral  lesion.  This  affection  is  generally  met  with  in  old  people 
with  prostatic  disease,  and  it  may  be  associated  with  symptoms  caused 
by  aiuemia  of  the  cord  from  disease  of  the  bloodvessels — vascular 
sclerosis — so  that  it  is  not  always  easy  to  determine  the  share  each  lesion 
takes  in  the  production  of  the  symptoms.  The  paraWtic  symptoms  are 
sometimes  caused  by  remote  irritation.  The  most  striking  examples 
of  paralysis  from  remote  irritatiiin  are  afforded  by  those  cases  in  which 
a  paraplegia,  or  even  a  paralysis  of  the  upper  extremities  suddenly 
disappears  on  the  expulsion  of  a  tape,  or  of  lumbricoid  worms.  The 
paralyses  which  result  from  injury  of  remote  parts  are  well  illustrated 
by  several  cases  which  occurred  during  the  American  war.  The  case 
of  a  soldier  is  reported  by  S.  Weir  Mitchell,  who  had  received  a  bullet 
wound  on  the  right  side  of  the  neck,  which  wounded  the  pharynx  and 
fractured  the  hyoid  bone,  but  did  not  implicate  any  important  nerve 
trunk.  The  injury  was  immediately  followed  by  paralysis  of  both 
upper  extremities ;  the  left  extremity  recovered  rapidly,  and  the  right 
improved  considerably  but  remained  feeble. 

In  another  case  reported  by  the  same  author,  a  wound  in  the  soft 
parts  of  the  thigh  which  did  not  injure  any  large  nerve  trunk,  was 
followed  by  right-sided  hemianalgesia  and  paralysis  of  all  the  four  ex- 
tremities. The  left  arm  recovered  rapidly,  but  the  improvement  in  the 
other  limbs  was  only  slow,  and  the  hemianalgesia  persisted. 

Neuritis  sometimes  gives  rise  to  paralysis  not  only  of  the  muscles 
supplied  by  the  affected  nerve  itself,  or  by  nerves  derived  from  the  same 
plexus,  but  also  to  paralysis  of  muscles  supplied  by  nerves  derived  from 
the  plexus  of  the  opposite  side  or  from  a  different  plexus  altogether. 
This  form  of  paralysis  is  caused  by  a  secondary  myelitis  set  up  by  tlie 
diseased  nerve.  This  condition  is  well  illustrated  by  a  remarkable  case 
reported  by  Charcot  and  Fere,  in  which  the  sciatic  nerves  Avere  injured 
by  a  severe  blow  over  the  point  of  their  emergence  from  the  pelvis. 
At  first  the  patient  suffered  from  the  usual  symptoms  of  inflammation  of 
the  sciatic  nerves.  At  the  end  of  three  months  after  the  injury,  lioth 
lower  extremities  were  so  feeble  that  the  patient  was  unable  to  maintain 
the  erect  posture,  and  then  there  was  also  an  involuntary  passage  of  the 


424  ATROPHIC    PARALYSES. 

urine  and  feces  and  loss  of  virile  power.  A  careful  examination  of  the 
patient  ten  months  after  the  injury  showed  that  all  the  muscles  supplied 
by  the  left  sciatic  nerves  were  paralyzed  and  atrophied,  and  manifested, 
to  a  marked  degree,  the  "  reaction  of  degeneration,"  these  muscles  being 
probably  affected  by  in^jury  of  the  different  fibres  of  the  nerves.  In  addi- 
tion to  paralysis  of  these  muscles  on  the  left  side,  the  corresponding 
muscles  of  the  right  limb  were  also  feeble  and  emaciated,  but  they  only 
gave  the  slightest  form  of  the  "reaction  of  degeneration,"  while  the 
muscles  supplied  by  the  left  superior  gluteal  nerve,  which  received  no 
direct  injury,  were  also  paralyzed  and  atrophied  and  manifested  the 
"  reaction  of  degeneration."  The  muscles  supplied  by  the  anterior 
crural  and  obturator  nerves  were  not  paralyzed  on  either  side.  The 
presence  in  this  case  of  paralysis  of  the  sphincters,  of  the  muscles  of 
the  right  lower  extremity,  and  of  the  gluteus  medius  and  minimus  of 
the  left  side  shows  conclusively  that  a  consecutive  myelitis  of  the  gray 
substance  was  set  up  by  the  local  injury  to  the  nerves.  The  excess  of 
the  patellar  tendon-reaction  on  the  right  side  is  explained  by  Charcot 
by  supposing  that  the  ganglion  cells  connected  with  the  anterior  crural 
nerve  were  maintained  in  a  state  of  irritation. 


CHAPTER    YII. 

ATROPHIC  PARALYSES  [contiaued). 
IV.  SPINAL  ATROPHIC  PARALYSES  (POLIOMYELOPATHIES). 

1.  Paralysis  Ascendens  Acuta  (Acute  Ascending  Paralysis, 
Landry's  Paralysis). 

Etiology. — Acute  ascending  paralysis  often  begins  in  the  absence  of 
any  recognizable  predisposing  cause,  but  it  is  thought  likely  that  syphi- 
litic infection  and  rheumatism  may  develop  a  liability  to  it.  Men  are 
more  frequently  attacked  than  women,  and  the  majority  of  cases  have 
occurred  between  twenty  and  forty  years  of  age.  The  exciting  causes 
are  exposure  to  cold,  suppression  of  menses,  and  convalescence  from 
acute  disease,  such  as  typhoid  fever,  variola,  and  pleurisy. 

SymiJtoms. — Premonitory  symptoms  consisting  of  slight  fever,  shoot- 
ing pains  in  the  back  and  limbs,  formication  and  numbness  in  the  feet 
and  finger-tips,  and  a  feeling  of  great  weariness,  debility,  and  general 
discomfort  may  be  present  several  days  before  the  occurrence  of  paral- 
ysis. The  characteristic  symptoms  of  the  disease  now  declare  them- 
selves by  a  paralysis  which  begins  in  the  muscles  of  the  feet  and  spreads 
upwards  to  those  of  the  thigh.  The  paralysis  progresses  with  so  much 
rapidity  that  in  a  few  days  the  lower  extremities  may  be  completely 
paralyzed,  and  the  limbs  lie  flaccid  and  pow^erless  in  any  position  in 
which  they  may  be  placed,  and  without  offering  the  slightest  opposition 
to  passive  movements. 

The  paralysis  continues  to  advance  steadily  upwards,  the  muscles  of 
the  trunk  are  invaded,  and  the  patient  is  unable  to  sit  up  in  bed ;  the 
small  muscles  of  the  hand  are  probably  the  next  to  be  attacked,  and 
delicate  manipulations,  like  those  of  writing,  become  impossible ;  the 
muscles  of  the  upper  arm  and  shoulder  are  successively  invaded;  the 
acts  of  urination,  defecation,  and  respiration  are  now  rendered  increas- 
ingly difficult  by  the  progressive  paralysis  of  the  abdominal  and  inter- 
costal muscles;  and  when  the  muscles  of  the  tongue,  lips,  pharynx, 
and  oesophagus  become  implicated  a  fatal  termination  is  near. 

A  considerable  degree  of  emaciation  may  occur  in  this  disease  as  in 
other  acute   affections,  but  the  paralyzed  muscles  do  not   undergo  n 


426  ATEOPHIC    PARALYSES. 

rapidly  progressive  atrophy,  and  with  rare  and  doubtful  exceptions  the 
electric  excitability  of  the  paralyzed  nerves  and  muscles  remains 
normal.  Reflex  action,  -which  is  preserved  or  occasionally  increased 
during  the  first  few  days  of  the  disease,  becomes  diminished  and  finally 
extinguished.  The  patellar  tendon-reactions  have  been  found  absent 
at  an  early  period  of  the  disease  in  those  cases  in  which  the  state  of 
these  reactions  has  been  tested. 

The  sensory  disorders  consist  merely  of  numbness  and  tingling  in 
the  fingers  and  toes,  but,  as  a  rule,  the  cutaneous  sensibility  is  found  to 
be  normal  on  objective  examination,  although  occasionally  a  slight 
diminution  of  tactile  sensibility  has  been  observed  at  the  periphery  of  the 
extremities.  The  pupils  are  sometimes  unequal,  and  towards  the  end 
the  pulse  is  very  frequent.  The  functions  of  the  bladder  and  rectum 
are  usually  unaffected,  there  are  no  bedsores,  the  general  health  is  often 
good,  and  the  intellect  is  clear  throughout  the  whole  course  of  the 
disease.  The  disease,  as  Ave  have  seen,  generally  begins  in  the  lower 
extremities,  but  in  some  cases  it  begins  in  the  upper  extremities,  or, 
rarely,  in  the  region  of  distribution  of  the  bulbar  nerves,  and  then  it 
pursues  a  descending  course. 

The  duration  of  the  affection  is  somewhat  variable.  In  some  cases 
it  terminates  fatally  in  the  course  of  two  or  three  days,  while  occasion- 
ally it  lasts  from  two  to  four  weeks,  the  average  of  fatal  cases  being 
from  eight  to  twelve  days.  Death  is  caused  by  arrest  of  res])iration 
subsequent  to  implication  of  the  bulbar  nerves.  The  disease  may  end 
in  recovery.  It  may  cease  to  progress  at  any  stage  of  its  development, 
and  even  after  the  cranial  nerves  are  implicated  the  case  must  not  be 
regarded  as  altogether  hopeless.  In  favorable  cases  improvement  begins 
at  an  early  period  of  the  disease,  the  parts  last  attacked  being  the  first 
to  recover. 

2.  Poliomyelitis  Axterior  Acita  (Kiss.maul)  (Acute  Inflam- 
mation OF  THE  Anterior  Gray  Horns,  Acute  Atrophic 
Spinal  Paralysis). 

Etiology. — This  affection  is  most  frequently  met  with  in  childhood, 
the  disease  appearing  between  the  ages  of  six  months  and  three  years 
in  thirty-two  out  of  forty-four  cases  observed  by  West.  It  may,  how- 
ever, occur  at  so  early  an  age  as  ten  days,  and  a  disease  essentially 
the  same  occurs  in  the  adult.  Heine  asserts  that  the  disease  occurs  in 
the  healthiest  children,  and  that  neither  sex  nor  hereditary  predisposi- 
tion  appears  to   exercise  any  influence  in  its  causation.  "  It  appears, 


SPIXAL    ATROPHIC    PARALYSES.  427 

according  to  Drs.  Bai-low  and  Wharton  Sinklcv,  to  be  more  common 
during  the  summer  than  the  winter  months. 

Injuries  of  various  kinds  are  often  said  to  be  the  cause  of  tlie  disease, 
and  nurses  are  fi-equently  blamed  unjustly  by  parents  who,  unalde  to 
believe  that  such  a  striking  phenomenon  as  paralysis  can  occur  sud- 
denly without  appreciable  cause,  imagine  that  the  child  has  been  lamed 
by  a  fall  through  the  carelessness  of  its  attendant.  The  most  usual 
exciting  causes  are  painful  dentition,  and  exposure  to  cold,  more  espe- 
cially when  the  body  is  overheated,  and  the  affection  often  occurs  in 
children,  and  occasionally  in  the  adult,  during  or  soon  after  an  attack 
of  measles,  scarlatina,  smallpox,  typhus,  and  other  acute  affections. 

Syyiqjtoms. — Although  this  disease  is  essentially  the  same  in  children 
as  in  adults,  yet  the  symptoms  differ  so  much  in  the  tAvo  as  to  demand 
separate  description.  The  disease  will  be  first  described  as  it  occurs  in 
children. 

a.  Infantile  Sjnnal  Atrophic  Paralym. 

It  Avill  conduce  to  clearness  if,  like  Laborde,  we  divide  the  clinical 
history  of  this  affection  into  the  periods  of  (1)  invasion ;  (2)  remission : 
(3)  regression  of  paralytic  ])lienomena ;  (4)  atrophy  with  deformities. 
It  must,  however,  be  remembered  that  these  ])eriods  overlap,  and  that 
this  subdivision  is  merely  adopted  for  the  sake  of  convenience. 

(1)  The  Period  of  Invasion. — The  disease  is  commonly  ushered  in 
by  a  more  or  less  intense  fever,  which  is  often  preceded  l)y  general 
malaise,  pain  in  the  head  or  in  the  back,  mental  irritaljility,  fretfulness, 
and  startings  of  the  limbs.  As  a  rule,  the  fever  is  of  short  duration, 
lasting  only  from  one  to  two  days.  In  some  cases  it  passes  off  in  a 
few  hours,  while  in  others  it  continues  from  fourteen  to  sixteen  days, 
or  even  longer.  As  the  fever  increases  the  cerebral  symptoms  become 
more  pronounced,  confusion  of  ideas  and  slight  somnolency  are  ob- 
served, and  the  child  may  become  unconscious,  or  delirium  of  varying 
degrees  of  intensity  may  supervene.  The  disease^  was  ushered  in  by 
convulsions  in  thirty  out  of  seventy  cases  collected  by  Duchenne.  these 
convulsions  being,  most  probably,  the  ordinary  eclamptic  attacks  which 
so  frequently  precede  every  acute  febrile  disease  in  childhood.  All 
general  symptoms  are  sometimes  absent ;  the  child  is  put  to  bed  appar- 
ently in  good  health,  and  is  found  paralyzed  in  the  morning. 

(2)  The  Period  of  Remission. — After  the  initial  symptoms  have  sub- 
sided it  is  observed  that  the  patient  is  unable  to  move  one  or  more  of 
his  limbs,  or  the  paralysis  may  not  attract  attention  until  the  child  is 


428  ATKOPHIC    PARALYSES. 

taken  out  of  bed  for  some  purpose  and  then  the  relaxed  and  helpless 
condition  of  the  affected  extremities  can  hardly  fail  to  be  noticed.  The 
paralysis  is  probably  never  fully  developed  at  once  ;  it  increases  gradually 
and  reaches  its  maximum  extent  and  degree  in  the  course  of  a  few 
hours,  in  a  day  or  two,  and  occasionally  not  until  a  longer  period  has 
elapsed.  Relapses  sometimes  occur.  After  a  first  attack  one  limb  is 
paralyzed  and  a  few  days  afterwards,  during  which  rapid  improvement 
has  been  taking  place,  the  child  is  seized  with  a  second  febrile  attack 
and  other  limbs  become  paralyzed.  A  case  is  reported  by  Laborde  in 
which  the  paralysis  did  not  become  permanently  established  until  the 
third  attack. 

The  distribution  of  the  paralysis  is  very  variable.  It  often  involves 
not  only  the  four  extremities,  but  also  the  muscles  of  the  vertebral 
column,  and  even  the  intercostal  muscles  and  those  of  the  neck  are  not 
always  spared.  Sometimes  the  lower  extremities  alone  are  paralyzed, 
but  the  upper  extremities  are  seldom  exclusively  affected.  The  paralysis 
assumes  in  some  cases  the  form  of  a  hemiplegia,  and  in  these  the  side 
of  the  neck,  of  the  face,  and  of  the  tongue  may  be  implicated  at  first 
and  may  on  rare  occasions  remain  permanently  paralyzed. 

Sensory  disorders  are  almost  entirely  absent  during  the  whole  course 
of  the  disease.  At  the  outset  patients  may  complain  of  pains  and 
various  parc^sthesicTe,but  these  symptoms  are  of  short  duration.  A  certain 
degree  of  cutaneous  hypertesthesia  or  rather  hyperalgesia  has  been 
described  as  being  present  during  the  febrile  stage,  but  this  tenderness 
to  touch  probably  depends  upon  affections  of  deeper  structures,  such  as 
rheumatic  inflammation  of  joints.  The  cutaneous  sensibility  is  some- 
times blunted  in  the  paralyzed  extremities  in  old  standing  cases,  but 
this  probably  depends  upon  underlying  nutritive  and  vascular  changes. 

Reflex  action  is  completely  lost  in  all  the  muscles  Avhich  are  severely 
paralyzed  and  it  is  much  lowered  or  temporarily  extinguished  in  the 
muscles  which  are  slightly  affected. 

The  tendon-reactions  are  also  absent  in  the  paralyzed  muscles. 

The  functions  of  the  bladder  and  rectum  are  rarely  affected.  During 
the  first  days  there  may  be  retention,  but  more  frequently  there  is  in- 
continence, and  the  stools  may  be  passed  involuntarily.  These  disorders 
disappear  in  from  three  to  eight  days  from  the  commencement,  except 
in  young  children,  in  whom  a  slight  incontinence  of  urine  may  remain 
for  some  time. 

(3)  The  Period  of  Regression. — After  a  certain  time,  which  varies 
from  a  few  days  to  a  few  weeks,  some  of  the  paralyzed  muscles  begin 
to  improve,  and  in  a  few  cases  complete  recovery  takes  place.  The 
cases  which  recover  have  been  described  by  Kennedy  under  the  name 


SPINAL    ATEOl'HIC    PARALYSES.  429 

temporary  spinal  2)arali/sis.  But,  as  a  rule,  only  some  of  the  muscles 
are  completely  restored,  while  the  rest  remain  permanently  paraly/.ed. 
When  the  paralysis  is  general  it  often  happens  that  the  upper  half  of 
the  body  is  the  first  to  shoAv  signs  of  amendment,  the  paralysis  disap- 
pearing rapidly  from  the  neck,  upper  extremities,  and  trunk,  and 
becoming  restricted  to  the  lower  extremities.  This  improvement,  which 
Laborde  calls  the  period  of  first  regression,  is  followed  after  a  variable 
interval  of  time  by  a  second  period  of  amendment,  which  the  same 
author  calls  the  period  of  second  regression.  During  the  second  re- 
gression some  of  the  muscles  of  the  lower  extremities  undergo  a  pro- 
gressive improvement  and  one  limb  may  be  restored  to  full  motor  power, 
while  one  or  more  of  the  muscular  groups  of  the  other  limb  may  remain 
permanently  affected,  particularly  the  anterior  and  external  group  of 
the  leg.  In  some  cases  improvement  takes  place  from  below  upwards 
instead  of  from  above  downwards,  and  then  the  paralysis  becomes 
permanently  localized  in  a  superior  extremity,  or  occasionally  in  the 
trunk  or  neck.  The  permanently  paralyzed  muscles  are  implicated  in 
groups  according  as  they  are  associated  in  their  action,  and  not  in  accord- 
ance with  the  peripheral  distribution  of  their  motor  nerves. 

(4)  Tlu-  Period  of  Atrophy  <md  Deformities. — All  the  muscles 
which  are  severely  paralyzed  become  the  subjects  of  a  rapidly  p>ro- 
gressive  atrophy,  and  even  those  which  are  but  slightly  affected  Avaste 
to  some  extent,  but  soon  recover.  The  atrophy  becomes  well  marked 
in  the  course  of  a  few  weeks,  in  the  muscles  which  are  severely  affected, 
and  after  a  time  they  become  so  attenuated  that  the  bones  seem  to  under- 
lie the  skin.  Sometimes  the  muscular  atrophy  is  masked  by  the  accu- 
mulation of  fat  in  the  connective  tissue,  and  consequently  the  loss  of 
volume  is  not  always  a  trustworthy  test  of  the  degree  to  which  the 
muscle  has  become  atrophied. 

The  electrical  reactions  of  the  affected  nerves  and  muscles  may  vary 
from  a  simple  diminution  of  the  normal  reactions  to  the  partial  or  the 
complete  reaction  of  degeneration.  It  was  first  shown  by  Duchenne 
that  the  faradic  irritability  of  both  nerves  and  muscles  sinks  quickly  in 
those  which  are  severely  attacked,  and  becomes  lost  in  them  on  the 
seventh  day  or  during  the  course  of  the  second  week.  He  laid  it  down 
as  a  rule  that  all  the  paralyzed  muscles  in  which  the  faradic  irritability 
is  only  more  or  less  diminished  during  the  course  of  the  second  week 
do  not  remain  permanently  paralyzed,  and  that  the  restoration  is  the 
more  prompt  and  complete  the  less  the  faradic  irritability  is  diminished. 

Arrest  of  development  of  the  osseous  system  often  occurs,  and  it  may 
be  altogether  out  of  proportion  to  the  degree  in  which  the  muscles  arc 
paralyzed.     The  greater  part  of  the  muscles  of  a  limb  nay.  indeed,  be 


480  ATROPHIC    PARALYSES. 

lost  while  the  bones  are  almost  entirely  unaffected,  and,  conversely,  a 
limb  may  be  considerably  shortened  while  only  one  or  two  muscles  are 
atrophied.  The  paralyzed  lower  extremity  may  be  found  from  two  to 
six  inches  shorter  than  the  corresponding  healthy  limb,  and  the  upper 
extremity  may  be  similarly  affected,  although  not  generally  to  the  same 
degree.  The  long  bones  are  thinner  than  normal ;  they  are  porous, 
friable,  and  yielding ;  their  epiphyses  and  processes  grow  smaller  and 
less  distinct ;  the  paralyzed  hand  or  foot  is  shorter,  narrower,  and  thinner 
than  the  sound  one  ;  and  even  the  pelvis  may  be  arrested  in  its  develop- 
ment. 

The  joints  become  unusually  movable,  partly  from  disappearance  of 
the  articular  extremities  of  the  bones  and  partly  from  relaxation  and 
stretching  of  their  ligaments,  and  occasionally  the  changes  undergone 
are  so  great  that  the  patient  is  able  to  dislocate  a  joint  without  experi- 
encing any  discomfort. 

The  shin  of  the  affected  extremity  is  flabby  an<l  so  inelastic  that  it 
retains  for  a  long  time  slight  pressure  marks,  such  as  that  made  by  the 
stocking.  The  surface  of  the  limbs  is  of  a  mottled  or  bluish  color,  it 
is  remarkably  cold  to  the  touch,  and  in  old  cases  its  tem})erature  may 
be  from  5°  to  12°  F.  lower  than  that  of  the  corresponding  healthy 
limb.  The  skin  is  liable  to  chilblains,  and  indolent  ulcers  form  on 
slight  provocation,  these  nutritive  changes  being  accompanied,  and 
probably  caused  by  a  diminution  in  the  calibre  of  the  arteries. 

The  deformities  occurring  in  the  affected  limbs  give  to  this  disease 
some  of  its  most  characteristic  features.  Some  pathologists  believe 
that  the  deformities  are  produced  by  the  predominant  action  of  the 
healthy  muscles,  the  normal  tonus  being  destroyed  in  the  affected 
muscles,  but  Volkmann  asserts  that  the  deformity  is  produced  mainly 
by  the  weight  of  the  limb  itself,  because  the  position  generally  assumed 
by  the  foot  is  only  a  higher  degree  of  that  which  it  assumes  when  un- 
supported and  left  free  from  the  action  of  the  muscles.  The  influence 
of  gravity  on  the  position  of  the  limb  ought  certainly  not  to  be  ignored, 
but  the  position  assumed  by  the  foot  in  talipes  calcaneus  when  the 
muscles  of  the  calf  are  paralyzed  shows  that  gravity  is  not  the  only, 
perhaps  not  the  chief,  force  which  is  operative  in  the  production  of 
these  deformities.  Two  other  factors,  at  least,  must  be  taken  into 
account.  The  first  is  that  the  paralyzed  muscles  often  permit  the  limb 
to  assume  a  position  in  which  the  ends  of  their  healthy  antagonists  are 
more  or  less  permanently  approximated,  and  the  latter  consequently 
become  permanently  shortened  by  undergoing  "adapted  atrophy." 
The  second  factor  is  that  the  paralyzed  muscles  themselves  may  become 
permanently  shortened   either  from  arrested  development  or  from  pro- 


SFIXAL    ATROPHIC    PARALYSES.  431 

liferation  and  subsequent  retraction  of  their  connective  tissues.  Of  all 
the  deformities  which  occur  in  infantile  paralysis,  talipes  e(iuinus  and 
e([uino-varus  are  the  most  frequent,  because  the  muscles  most  frequently 
paralyzed  are  the  long  extensors  of  the  toes,  the  tibialis  anticus,  the 
extensors  of  the  great  toes,  and  the  peronei  muscles.  When  the  anterior 
group  and  the  adductors  of  the  foot  are  affected  at  the  same  time  talipes 
equino-valgus,  and  when  the  muscles  of  the  calf  alone  are  affected  talipes 
calcaneus  is  produced,  but  this  form  is  exceedingly  rare,  and  simple 
talipes  varus  is  of  still  rarer  occurrence.  Another  common  deformity 
is  the  "'pes  cavus" — "talus  pied  creux"  of  the  French,  in  which  the 
sole  is  hollowed  and  the  instep  is  rendered  prominent.  Duchenne  thinks 
it  is  caused  by  a  more  or  less  complete  paralysis  of  the  muscles  of  the 
calf,  along  with  simultaneous  contraction  of  the  flexors  of  the  foot,  either 
the  long  flexors  of  the  toes  or  the  long  peroneus.  The  great  laxity  of 
the  ligaments  allows  the  foot  to  become  bent  upon  itself  from  the  trans- 
verse tarsal  joint  when  the  foot  is  unsupported,  but  when  it  is  place<l 
upon  the  ground  it  assumes  the  form  of  ''flat-foot." 

Various  deformities  occur  in  the  inferior  extremity,  according  to  the 
extent  and  localization  of  the  paralysis.  The  anterior  and  internal 
muscles  of  the  thigh  are  those  most  usually  affected  above  the  knee, 
and  then  the  predominant  action  of  the  flexors  of  the  leg  on  the  thigh 
maintains  the  leg  in  a  permanent  condition  of  partial  flexion  (genu 
recurvatum),  while  the  thigh  is  likewise  abducted.  This  deformity  is 
always  associated  with  flexion  of  the  thigh  on  the  body,  and  talipes 
equino-varus  (Fig.  137).  All  the  muscles  of  both  legs  are  sometimes 
paral^'zed,  so  that  the  patient  is  compelled  to  walk  on  his  knees,  drag- 
ging his  small,  thin  legs  after  him.  In  still  more  aggravated  cases  the 
muscles  of  both  legs  and  thighs  are  permanently  paralyzed,  so  that  the 
small,  flexible  limbs  dangle  about  like  the  limbs  of  a  doll  (jambe  de 
polichinelle).  Curvatures  of  the  vertebral  column  generally  result  in 
infantile  paralysis  from  the  attitudes  imposed  by  other  deformities,  but 
occasionally  the  curvature  is  caused  more  or  less  directly  by  the  paral- 
ysis. Of  the  direct  curvatures  lordosis  is  the  most  frequent  and 
important;  it  is  caused  by  partial  paralysis  of  the  sacro-spinal  muscles, 
and  in  order  to  prevent  the  permanent  bending  forwards  of  the  body, 
by  the  predominant  action  of  the  flexors,  the  patient  voluntarily  throws 
the  trunk  backwards,  so  that  the  weight  of  the  trunk  is  borne  by  the 
flexors,  while  the  tension  is  taken  off  the  partially  paralyzed  extensors. 
In  this  form  of  lordosis  the  pelvis  is  pushed  forwards,  and  the  buttocks 
become  less  prominent  than  in  health. 

The  deformities  of  the  upper  extremities  are  much  less  frequent  and 
serious   than   those  of  the   lower    extremities.      The  muscles  of  the 


432 


ATEOPHIC    PARALYSES. 


shoulder,  and  particularly  the  deltoid,  are  the  most  usual  subjects  of 
paralysis  and  atrophy  in  the  upper  extremity.  In  the  severer  forms  of 
paralysis  of  the  muscles  about  the  shoulder-joint  the  humerus  becomes 
separated  from  the  glenoid  cavity,  so  that  a  dislocation  is  readily  pro- 
duced or  may  occur  spontaneously,  the  arm  hangs  powerless  by  the 

Fig.  137. 


Case  of  Ixkaxtile  Paralysis  (genu  becvbvatum).    (After  Laumitii). 

side,  and,  to  use  the  apt  comparison  of  Heine,  dangles  about  like  the 
loose  end  of  a  flail.  The  distortions  of  the  forearm  and  hand  are  not 
so  frequent  or  important  as  to  require  description. 

The  general  health  of  the  patient  is  not  interfered  with  in  this  dis- 
ease; the  organic  functions  are  "well  performed  and  the  patient  may 
live  to  extreme  old  age. 


b.  Acute  Atrophic  Spinal  Paralysis  of  Adults. 

Acute  atrophic   spinal  paralysis  of  adults   is  essentially  the  same 
disease  as  acute  atrophic  spinal  paralysis  of  infants.     The  differences 


SPIXAL    ATROPHIC    I'ARALYSES.  433 

between  the  clinical  features  of  the  two  affections  result  from  the  fact? 
that  the  brain  of  the  adult  does  not  respond  so  readily  to  the  acute 
symptoms  of  the  initial  stage  as  that  of  the  infant ;  that  the  adult 
organism  is  not  so  liable  to  fever  as  that  of  the  infant ;  and  that  in  the 
adult  the  ligaments  and  joints  being  fully  developed  offer  greater  resist- 
ance to  the  resulting  deformities  than  do  those  of  infants.  The  disease 
begins  by  pain  in  the  back  and  extremities,  parnesthesia,  and  more  or 
less  fever.  In  addition  there  may  be  headache,  vomiting,  somnolency, 
or  even  slight  delirium,  but  convulsions  have  never  been  observed. 

The  paralysis  is  developed  more  or  less  rapidly,  generally  in  the 
course  of  a  few  hours ;  and,  as  in  the  case  of  children,  it  is  more  or  less 
widely  spread,  complete,  and  associated  with  more  or  less  flaccidity  of 
the  paralyzed  muscles.  Reflex  action  is  either  much  lowered  or  abolished 
in  the  paralyzed  muscles,  but  may  be  retained  in  those  which  are  slightly 
affected.     Temporary  weakness  of  the  bladder  may  be  present  at  first. 

The  initial  general  symptoms  pass  off"  in  a  fcAV  days ;  soon  afterwards 
the  paralytic  symptoms  begin  to  improve,  and  complete  restitution  of 
motor  power  may  take  place  in  the  course  of  some  weeks  or  occasionally 
not  until  the  lapse  of  nine  months,  these  cases  forming  the  temporary 
spinal  paraJi/sis  of  adults.  But  the  restoration  of  motor  power  is,  as 
a  rule,  partial,  the  muscles  which  remain  permanently  paralyzed  suffer- 
ing a  rapidly  progressive  atrophy  as  in  the  case  of  children  and  affording 
the  usual  evidences  of  the  reaction  of  degeneration.  The  skin  becomes 
loose,  flabby,  and  inelastic,  and  the  affected  extremities  are  cold  and 
cyanotic. 

Paralysis  of  one  extremity  is  most  commonly  met  w'ith  in  infants, 
but,  according  to  Miiller,  paralysis  of  the  four  extremities,  or  of  Ijoth 
the  lower  extremities,  occurs  more  frequently  in  adults.  Out  of  forty- 
seven  cases  collected  by  him  tlie  paralysis  implicated  all  the  extremities 
in  twenty-two,  both  lower  jextremities  in  eleven,  both  upper  extremities 
in  three,  an  upper  and  lower  extremity  of  the  same  side  in  one,  ami  an 
upper  and  lower  extremity  of  opposite  sides  in  one.  The  right  upper 
extremity  was  paralyzed  in  one,  the  left  in  two,  the  right  inferior  in  two, 
and  the  left  inferior  in  one  case. 

The  sensory  disorders  which  may  have  existed  at  the  beginning  soon 
subside,  and  the  sensibility  becomes  normal ;  the  sexual  functions  are 
throughout  unaffected  :  there  are  no  bedsores,  and  the  general  health  is 
good. 

Paralytic  contractions  supervene  with  their  resulting  deformities,  but 
never  attain  the  same  degree  as  in  children,  because  the  joints  and 
ligaments  in  adults  are  resistant  and  the  long  bones  have  attained  their 
full  development. 

28 


434  ATROPHIC    PARALYSES. 

3.  Poliomyelitis  Anterior  Chronica  (Chronic  Atrophic 
Spinal  Paralysis). 

Etiology. — The  causes  of  this  disease  are  exceedingly  obscure ;  it 
was  thought  that  adults  were  alone  attacked,  but  it  is  now  known  that  it 
occurs  in" children.  The  most  frequent  exciting  causes  are  injuries, 
such  as  a  fall  on  the  back  or  hip,  exposure  to  severe  cold,  damp  dwellings, 
and  alcoholic  and  sexual  excesses. 

Symptoms. — The  disease  usually  begins  with  a  feeling  of  lassitude 
and  fatigue  in  walking,  pain  and  stiffness  in  the  loins  and  lower  ex- 
tremities, slight  fever,  gastric  disturbance,  headache,  and  various  par- 
lesthesiffi,  such  as  tingling  and  formication  of  the  feet  and  hands.  After 
a  time  distinct  muscular  weakness  is  felt  in  one  or  both  lower  extremities, 
which  gradually  increases  until  complete  paralysis  is  established.  The 
intrinsic  muscles  of  the  foot,  and  the  extensors  of  the  toes  and  foot  are 
the  first  to  be  affected,  and  subsequently  the  muscles  of  the  calf,  the 
flexors  of  the  thigh  on  the  trunk,  the  flexors  and  extensors  of  the  leg 
on  the  thigh,  and  the  extensors  of  the  thigh  on  the  body  become  suc- 
cessively invaded.  The  disease  pursues  its  ascending  course  and  the 
muscles  of  the  back  and  abdomen  become  paralyzed,  so  that  the  patient 
is  no  longer  able  to  sit  up  in  bed,  and  expiratory  acts  like  coughing  and 
sneezing,  as  well  as  urination  and  defecation,  are  rendered  difficult  and 
inefiective.  As  the  intercostal  muscles  are  gradually  attacked,  it  is  seen 
that  the  breathing  becomes  more  and  more  diaphragmatic,  and  at  the 
same  time  the  small  muscles  of  the  hand  show  signs  of  atrophy  while 
the  grasp  is  feeble  from  paralysis  of  the  long  flexors  of  the  fingers. 
The  flexors  of  the  forearm,  the  extensors  of  the  forearm,  the  supinators, 
and  the  muscles  of  the  arm  and  shoulder  are  next  attacked  in  succession. 
It  is  important  to  observe  that  in  this  disease  the  intercostal  muscles 
are  attacked  before  the  diaphragm,  and  the  intrinsic  muscles  of  the 
hand  and  the  flexors  of  the  fingers  before  the  extensors  of  the  forearm, 
this  mode  of  invasion  being  the  reverse  of  what  occurs  in  alcoholic  and 
lead  paralysis  and  other  forms  of  multiple  neuritis.  But,  although  the 
disease  usually  begins  in  the  lower  extremities  and  pursues  an  ascending 
march,  it  sometimes  begins  in  the  upper  extremities  and  pursues  a 
descending  course,  or  rather  pursues  an  ascending  and  a  descending 
course,  inasmuch  as  the  bulbar  nuclei  are  liable  to  be  invaded  as  well  as 
the  motor  cells  of  the  dorsal  and  lumbar  rejrions.  Althoudi  the  two 
lower  and  the  two  upper  extremities  are  usually  affected,  the  paralysis 
is  frequently  more  pronounced  on  one  side  of  the  body  than  on  the 
other.     The  paralyzed  muscles  are  soft  and  flaccid,  tension  is  not  pro- 


SPINAL    ATROPHIC    PARALYSES.  435 

voked  in  them  by  passive  movements  of  the  affected  extremities,  and 
they  undergo  rapid  atrophy.  The  calves  of  the  legs  become  converted 
into  loose  and  flabby  sacs,  the  muscles  of  the  thighs  and  gluteal  regions 
grow  thin  and  soft,  and  the  bones  of  the  lower  extremities  may  ulti- 
mately be  felt  immediately  underlying  the  skin,  while  scarcely  a  trace 
of  the  muscular  masses  is  left.  The  patient  now  lies  on  his  back  with 
the  various  segments  of  the  lower  extremities  extended  upon  one  another ; 
the  upper  extremities  lie  immovable  by  his  side  in  any  position  in  which 
they  may  be  placed ;  the  arms  and  forearms  become  greatly  emaciated 
from  disappearance  of  their  muscular  masses  ;  the  thenar  and  hypo- 
thenar  eminences  are  flattened ;  and  the  hands  assume  characteristically 
distorted  positions. 

Fibrillary  contractions  may  be  present  in  the  early  stages  of  the 
atroph}^,  but  these  soon  disappear.  Reflex  action  is  lost  at  an  early 
period  of  the  disease,  and  the  tendon-reactions  are  likewise  soon  abolished. 
The  electrical  reactions  of  the  paralyzed  nerves  and  muscles  are,  on  the 
whole,  the  same  as  those  met  with  in  acute  atrophic  spinal  paralysis, 
lieing  only  modified  to  some  extent  in  correspondence  with  the  slow 
development  of  the  former  disease  as  compared  with  the  latter.  A  case 
of  this  disease  came  under  my  observation  in  which  the  faradic  con- 
tractility of  the  paralyzed  nerves  and  muscles  was  at  first  much  increased 
during  the  early  stage,  but  it  was  completely  lost  after  a  few  weeks,  and 
then  the  galvanic  reactions  manifested  the  qualitative  changes  which 
characterize  the  "reaction  of  degeneration." 

The  sensory  disorders  consist  of  tingling  and  formication,  but  the 
cutaneous  and  muscular  sensibilities  are  found  to  be  normal  on  objective 
examination. 

The  skin  of  the  paralyzed  limbs  may  become  of  a  blue  color  and 
the  surface  may  be  cold,  while  the  lower  extremities  may  be  oedema- 
tous,  but  there  are  no  bedsores  nor  cutaneous  eruptions,  the  functions  of 
the  bladder,  rectum,  and  sexual  organs  remain  unaffected,  and  the 
general  health  is  satisfactory.  During  the  course  of  the  disease  the 
small  joints  of  the  hand  are  liable  to  become  swollen,  red,  and  painful, 
and  the  patient  may  be  covered  with  an  abundant  sour-smelling  per- 
spiration like  that  of  acute  rheumatism.  The  acute  symptoms  subside, 
but  the  joints  are  apt  to  remain,  to  some  extent,  permanently  deformed 
like  those  of  rheumatic  arthritis.  The  course  of  the  disease  is  variable, 
the  paralysis  may  supervene  suddenly  or  be  preceded  for  some  time  by 
premonitory  symptoms,  and  when  the  lower  extremities  are  the  first  to 
be  attacked,  the  upper  extremities  may  be  implicated  in  a  few  weeks  or 
not  until  the  lapse  of  months  or  years.  In  fatal  cases  death  is  usually 
caused  by  implication  of  the  bulbar  nuclei  and  respiratory  paralysis,  but 


436  ATROPHIC    PARALYSES. 

occasionally  it  results  from  exhaustion.  Very  frequently  the  disease 
becomes  arrested  in  its  upward  course,  and,  after  a  stationary  period  of 
variable  duration,  improvement  takes  place  in  the  muscles  which  Avere 
the  last  to  be  invaded.  During  recovery  the  electrical  reactions  return 
slowly  and  gradually  to  the  normal  formula.  Recovery  from  this  dis- 
ease is  not  often  complete.  Groups  of  muscles,  especially  the  anterior 
and  external  muscles  of  the  legs,  remain  paralyzed  and  atrophied,  and 
the  patient  is  partially  disabled  for  life. 


4.  Periependymal  Myelitis  (Syringomyelia,  Hydromyelia). 

Etiology. — The  causes  of  this  disease  are  the  same  as  for  other  forms 
of  myelitis. 

Symptoms. — This  affection  begins  somewhat  abruptly  by  paralysis  of 
some  muscular  groups,  the  patient  finding  suddenly  that  he  is  unable 
to  move  the  fingers,  hands,  or  more  rarely  an  entire  limb.  The  muscles 
lose  their  faradic  contractility,  and  become  atrophied  at  an  early  period 
of  the  disease,  and  the  affected  extremities  assume  distorted  positions. 
In  the  early  stage  of  the  disease  the  uniscles  may  manifest  fibrillary 
contractions,  and  occasionally  involuntary  movements  of  a  limb  or  of 
the  trunk  have  been  observed.  Patients  often  complain  of  vague  pains 
along  the  vertebral  column,  but  in  most  cases  there  are  no  other  sensory 
disorders.  In  some  cases,  however,  the  patient  suffers  from  numbness 
and  tingling  of  the  lower  extremities,  and  there  may  be  an  extensively 
diffused  anaesthesia,  as  in  a  case  recorded  by  Schiippel,  which  was  fre- 
quently exhibited  during  life  in  Niemeyer's  clinic.  An  ataxic  gait  has 
never  been  observed,  and  the  bladder  and  rectum  always  remain 
unaffected. 

The  course  of  the  disease  is  slow,  and  it  may  be  temporarily  arrested, 
or  may  even  regress,  and  then  the  atrophied  muscles  gradually  regain 
their  motor  power  and  volume,  but  relapses  are  liable  to  occur.  Tlie 
muscles  of  the  lower  extremity  most  fre(|uently  affected  are  the  flexors 
of  the  foot  on  the  leg,  and  of  the  thigh  upon  the  pelvis ;  and  of  the 
upper  extremities,  are  the  extensors  of  the  fingers  and  of  the  hand;  then 
the  small  muscles  of  the  hand,  and  lastly  the  flexors  of  the  forearm, 
and  the  muscles  of  the  arm  and  shoulder.  The  disease  pursues  an 
ascending  course  when  the  lower  extremities  are  the  first  to  be  para- 
lyzed, and  both  an  ascending  and  a  descending  course  when  the  upper 
extremities  are  attacked  first,  and  bulbar  paralysis  is  ultimately  liable 
to  supervene,  and  to  cause  death.  In  some  cases  the  paralytic  symp- 
toms pursue  a  rapidly  ascending  course,  and  the  disease  may  then  be 
mistaken  for  an  acute  ascending  paralysis. 


SPINAL    ATROPHJC    PARALYSES.  437 


5.  Progressive  Muscular  Atrophy. 

Etiolotjjj. — Hereditary  predisposition  is  generally  supposed  to  play  a 
very  important  part  in  the  production  of  progressive  muscular  atrophy, 
but  it  is  most  probable  that  the  cases  in  which  the  disease  appears  in 
numerous  members  of  the  same  family  really  belong  to  the  group  which 
Erb  has  described  under  the  name  of  the  "juvenile  form  of  progressive 
muscular  atrophy,"  a  group  which  is  more  allied  to  pseudo-hypertrophic 
paralysis  than  to  genuine  progressive  muscular  atrophy,  and  until  the 
two  groups  of  cases  are  separated  from  one  another  by  a  rigid  analysis, 
we  are  not  in  a  position  to  estimate  the  part  which  heredity  plays  in 
the  production  of  progressive  muscular  atrophy.  The  disease  attacks 
males  more  frequently  than  females,  the  proportion,  according  to  Fried- 
reich, being  one  hundred  and  forty-three  males  to  thirty-three  females. 
The  disproportion  between  the  sexes  probably  depends  on  men  being 
more  exposed,  than  women,  to  the  exciting  causes  of  the  disease. 

Progressive  muscular  atrophy  is  often  developed  during  convalescence 
from  acute  diseases,  such  as  typhus  fever,  measles,  acute  rheumatism, 
and  cholera,  and  it  occasionally  begins  in  Avomen  soon  after  parturition. 

Of  the  exciting  causes  of  the  disease  the  most  usual  are  excessive 
muscular  exertion,  exposure  to  cold  and  damp,  injuries  of  various 
kinds,  and  sexual  and  other  excesses. 

Symptoiiis. — The  invasion  of  progressive  muscular  atrophy  is  slow 
and  insidious,  and  the  disease  is  usually  in  existence  some  weeks  or 
months  before  its  presence  is  discovered.  The  patient  first  experiences 
some  difficulty  in  performing  certain  movements,  and  on  attention 
being  directed  to  the  aifected  limbs,  some  of  the  muscles  are  found  to 
be  more  or  less  wasted.  At  other  times,  especially  when  the  disease 
has  been  caused  by  exposure  to  cold,  the  mode  of  invasion  is  attended 
l)y  more  prominent  symptoms.  Paroxysmal  pains,  like  those  of  rheu- 
matism or  of  neuralgia,  are  felt  in  the  affected  limb  several  weeks  or 
months  before  the  atrophy  of  the  muscles  is  noticed,  and  when  once 
the  atrophy  begins  in  these  cases  it  proceeds  more  rapidly,  and  becomes 
more  generalized  than  in  the  painless  variety. 

The  disease  usually  begins  in  one  of  the  upper  extremities,  more 
commonly  in  the  right,  and.  the  first  muscles  to  be  attacked  are  either 
those  of  the  thenar  or  hypothenar  eminences,  the  interossei,  or  the 
muscles  about  the  shoulder.  It  will  be  shown  hereafter  that  the  cases 
in  which  the  atrophy  begins  in  the  muscles  of  the  loAver  extremities 
and  the  lumbar  muscles  are  most  probably  not  examples  of  true  pro- 
gressive paralysis.     Dui'ing  the  progress  of  the  disease  certain  muscles 


438 


ATROPHIC    PARALYSES. 


or  groups  of  muscles  are  attacked  while  their  neighbors  are  spared,  and 
the  healthy  and  less  atrophied  muscles  overcome  the  resistance  of  the 
more  diseased,  and  thus  produce  distortions,  which  are  rendered  more 
characteristic  by  the  wasting  of  the  muscles.  The  disappearance  of 
the  interossei  is  shown  by  the  deep  furrows  which  appear  between  the 
metacarpal  bones  ;  the  thenar  and  hypothenar  eminences  are  flattened, 
and  the  disappearance  of  the  muscles  of  the  palm  brings  into  view  the 
diverging  flexor  tendons  which  are  stretched  between  the  wrists  and  the 
bulging  bases  of  the  fingers.  The  deformity  produced  by  paralysis  of 
the  interossei  gives  to  the  hand  the  appearance  of  the  talons  of  a  bird 
of  prey,  and  consequently  it  has  been  called  the  claw-shaped  hand,  or 
main  en  griff e  (Fig.  138).     This  deformity,  however,  is  not  peculiar  to 

Fig   138. 


1-  Main  en  Guiffp:,  2. 

(1)  Hand,  Palmak  Surface.     (2)  Dousal  Surface.    (After  Duchenne.) 

A,  Wound  of  the  ulnar  nerve  ;  B,  Ends  of  the  metacarpal  bones ;  D,  Tendons  of  the  flexor 

subllmis  ;  C,  Muscles  of  the  ball  of  the  thumb. 

progressive  muscular  atrophy,  inasmuch  as  it  may  be  caused  by  injury 
of  the  ulnar  and  median  nerves. 

Atrophy  and  paralysis  of  the  opponens  and  abductor  pollicis  cause 
the  thumb  to  be  extended  and  abducted  when  the  flexors  of  the  hands 
and  fingers  are  afl'ected,  the  anterior  and  internal  aspects  of  the  fore- 
arm are  flattened,  and  when  the  extensors  of  the  hands  and  fingers  are 


SPINAL    ATROPHIC    PARALYSES.  439 

attacked  the  posterior  aspect  of  the  forearm  presents  a  thin  and  wasted 
appearance.  Atrophy  of  the  supinator  longus  gives  rise  to  a  flattening 
of  the  external  border  of  the  forearm.  When  the  disease  begins  in 
the  small  muscles  of  the  hand  and  ascends  gradually  towards  the  trunk, 
the  supinator  longus  is  often  the  only  muscle  of  the  forearm  which 
retains  its  plumpness,  but  when  the  disease  begins  in  the  muscles  of 
the  shoulder  and  extends  to  the  periphery,  the  external  border  of  the 
forearm  becomes  flattened  at  an  early  period  from  implication  of  the 
supinators. 

When  the  muscles  of  the  shoulders  are  affected  the  arms  may  hano- 
by  the  side  and  rather  in  front  of  the  patient  and  seem  as  if  they  were 
merely  attached  to  him  by  strings  and  did  not  belong  to  him ;  the 
natural  rounded  configuration  of  the  shoulder  is  replaced  by  a  hollow 
in  which  the  palm  of  the  hand  may  be  lodged  under  the  projecting 
acromial  and  coracoid  processes  of  the  scapula,  which  stand  out  in 
relief  The  biceps  and  the  other  muscles  of  the  arm  may  also  waste, 
so  that  the  limb  loses  its  roundness  and  becomes  flattened,  and  the 
humerus  appears  to  be  surrounded  merely  by  a  bag  of  skin.  When 
the  abdominal  muscles  are  affected,  the  lumbar  curve  is  greatly  ex- 
aggerated by  the  unopposed  action  of  the  erectors  of  the  spine,  and 
the  abdomen  is  loose  and  protruding,  but  the  thorax  is  held  well  for- 
wards, so  that  a  plumb-line  let  drop  from  the  most  prominent  of  the 
spinous  processes  of  the  vertebra  will  pass  well  within  the  sacrum. 
When  the  atrophy  is  unequally  distributed  oh  both  sides  of  the  body, 
scoliotic  or  kyphotic  bending  of  the  vertebral  column  is  produced. 
When  the  erectors  of  the  spine  and  the  extensors  of  the  thigh  are 
simultaneously  affected  the  resulting  deformities  and  the  gait  are  similar 
to  those  observed  in  pseudo-hypertrophic  paralysis  and  need  not  be  de- 
scribed here. 

Implication  of  the  muscles  of  the  lower  extremities  is  rare  except  in 
the  later  stages  of  the  disease,  but  when  they  are  attacked  the  various 
forms  of  paralytic  club-foot  may  appear. 

The  accessory  respiratory  muscles,  such  as  the  pectoralis  major, 
serratus  magnus,  and  trapezius,  are  frequently  invaded ;  and  although 
the  wasting  and  loss  of  power  of  these  muscles  do  not  directly  endanger 
life,  yet  they  may  do  so  indirectly,  inasmuch  as  a  slight  intercurrent 
attack  of  bronchitis  may  lead  to  asphyxia  from  the  inability  of  the 
patient  to  make  a  strong  expiratory  effort  to  clear  the  tubes  of  mucus. 
In  the  later  stages  of  the  affection  the  diaphragm  and  the  intercostal 
muscles  become  attacked,  expectoration  fails,  mucus  collects  in  the  tubes, 
and  the  patient  dies  asphyxiated.  In  other  cases  a  progressive  bulbar 
paralysis^  is  superadded  to  the  atrophy  of  the  other  muscles,  and  the 


440  ATKOPIIIC    PARALYSES. 

disease  is  then  generally  fatal  from  arrest  of  respiration  caused  by 
paralysis  of  the  centre  in  the  medulla.  The  loss  of  muscular  paralysis 
keeps  pace  with  the  atrophy,  and  is,  as  a  rule,  directly  in  proportion  to 
the  degree  of  the  latter,  and  so  long  as  any  muscular  fibres  are  left,  they 
can  be  made  to  contract  by  voluntary  efibrt.  For  a  long  time,  indeed, 
the  various  movements  are  capable  of  being  perfonned,  although  with 
diminished  poAver,  and  it  is  only  in  the  last  stage  of  the  disease  that 
complete  immobility  of  the  limb  is  produced.  When  once  a  muscle  is 
attacked,  it  wastes,  as  a  rule,  in  a  perfectly  uniform  manner,  but  in 
some  cases  a  portion  only  of  the  length  of  the  muscle  undergoes  atrophy, 
while  the  remainder  maintains  its  volume,  and  to  a  considerable  degree 
its  power  also. 

The  jihrUlary  contractions  of  the  affected  muscles,  consisting  of 
vibratory  tremors  or  quivering  of  the  fibres,  are  frequently  observed 
throughout  the  whole  active  stage  of  the  disease.  They  occur  spon- 
taneously, but  may  be  ])rovoked  by  gently  tapping  the  surface,  by 
exposing  to  air  parts  which  are  usually  covered,  by  electrical  excitation, 
and  by  active  or  passive  movements  of  the  affected  muscles.  These 
fibrillary  contractions  arc  sometimes  the  earliest  symptom  of  a  fresh 
advance  of  the  disease,  and  they  disappear  altogether  when  the  atrophy 
has  reached  an  extreme  degree,  or  when  its  progress  is  arrested. 
Tonic  or  clonic  contractions  of  entire  muscles  or  of  groups  of  muscles 
may  occasionally  occur,  which  are  accompanied  by  an  intense  pain 
like  that  of  cramp  at  the  calf.  During  the  stage  of  active  fibrillary 
contractions  the  idio-muscular  contractility  may  be  so  much  increased 
that  the  slightest  tap  on  the  tendons,  fasciic,  neighboring  bones,  or 
on  the  bellies  of  the  muscles  themselves  occasions  widely  diffused  con- 
tractions, such  as  are  frequently  observed  in  advanced  cases  of  acute 
phthisis.  When  the  muscles  of  the  upper  extremity,  for  instance,  are 
undergoing  active  atrophy  a  slight  tap  on  the  lower  end  of  the  radius 
may  cause  almost  the  whole  of  the  muscles  of  the  forearm  and  arm, 
as  w^ell  as  the  pectoral  muscles,  to  enter  into  contraction,  and  the 
forearm  may  be  jerked  upwards  just  as  occurs  in  cases  of  spasmodic 
paralysis ;  and  when  the  atrophy  invades  the  muscles  of  the  lower 
extremities  the  knee-jerk  may  be  so  lively  as  to  give  rise  to  considerable 
difficulty  in  diagnosis. 

The  cutaneous  reflex  actions  are  often  exaggerated  during  the  active 
stage  of  atrophy,  and  this  renders  still  greater  the  similarity  of  the 
affection  to  a  spasmodic  paralysis.  As  the  atrophy  advances,  the 
cutaneous  reflexes  and  tendon-reactions  become  diminished  and  finally 
disappear. 

The  electrical  reactions  of  the  paralyzed  muscles  may  also  be  at  first 


SPIXAl.    ATROPHIC    PARALYSE/     \  441 

/ 


increased.  During  tlie  active  stage  of  atrophy  fee]fl^ , //ctrical  currents 
either  passed  through  the  nerve  or  the  muscle  inttu^^fe  very  active  con- 
tractions, ahhough  their  energy  is  diminished  according  to  the  decree 
of  atrophy.  iVs  the  atrophy  advances  the  strength  of  current  required 
to  produce  a  minimum  contraction  becomes  greater  and  greater,  and 
after  a  time  the  qualitative  changes  in  the  galvanic  reactions  -which 
characterize  the  "  reaction  of  degeneration  "  ar,e  observed. 

The  sensory  disorders  of  progressive  mupcdlar  atrophy  are  of  sub- 
ordinate importance.  In  some  cases  the  raiiscular  disease  is  preceded 
by  paroxysms  of  pain  in  tlie  affected  parts,  which  sometimes  radiate 
along  the  branches  of  certain  nei'^es,  and  at  other  times  appear  to  have 
their  origin  in  the  sensory  nerves  of  the  muscles,  the  pain  being  then 
aggravated  by  compression  of  the  affected  muscles  or  by  passive  move- 
ments of  them.  A  moderate  degree  of  anaesthesia  may  be  present  in 
the  hands  and  tips  of  the  fingers  in  the  later  stages  of  the  disease,  -while 
complete  analgesia  of  circumscribed  areas  of  the  skin  is  not  uncommon, 
and  in  some  cases  the  area  of  analgesia  is  much  more  extensive  than 
that  of  the  atrophied  muscles.  The  farado-cutaneous  sensibility  may 
also  be  diminished,  and  the  patient  often  complains  of  sensations  of 
cold,  numbness,  formication,  and  other  parfesthesise  in  the  hands  and 
feet. 

The  vaso-motor  disturbances  consist  of  a  local  spasm  of  the  blood- 
vessels giving  rise  to  coldness  and  pallor  of  the  affected  parts,  -v\'hicli  is 
apt  to  be  followed  by  relaxation  of  the  vessels  and  consequent  warmth 
and  redness.  In  the  early  stages  of  the  disease  the  temperature  of  the 
affected  extremities  is  increased,  according  to  Frommann,  by  0.2°  or 
0.3°  C,  Avhile  in  the  later  stages  it  may  sink  3°  or  4°  C.  below  the 
normal.  In  the  later  stages  of  the  disease  the  patient  is  sometimes 
covered  -\yith  a  profuse  sweat  (hyperidrosis)  which  is  probably  due  to 
vaso-motor  paralysis. 

Tro-pliie  disorders  may  sometimes  occur  in  addition  to  the  muscular 
atrophy.  The  skin  is  sometimes  the  subject  of  atrophy,  but  never  to  a  very 
pronounced  degree.  In  the  early  stages  of  the  disease  the  patient  may  be 
attacked  with  painful  swellings  of  the  phalangeal  joints  (arthritis  nodosa), 
which  are  most  probably  related  to  the  arthropathies  of  tabes  dorsalis. 

Oculo-piqnllarij  symptoms,  consisting  of  paralytic  myosis  and  diminu- 
tion of  the  palpebral  fissures,  have  occasionally  ))een  observed ;  but  it  is  sur- 
prising how  rarely  these  phenomena  are  met  with  when  it  is  considered 
how  frequently  the  lesion  is  localized  in  the  spinal  cord  on  a  level  Avith 
the  cilio-spinal  region.  In  the  early  stage  of  progressive  muscular 
atrophy  the  patient  may  complain  of  chills,  and  there  may  be  a  con- 
tinuous, though  slight,  increase  of  temperature,  wliich  lasts  for  days 


\ 

\ 

442  ^  ATROPHIC    PAEALYSES. 

or  months.  T^S^Vebrile  condition  may  probably  be  due  at  times  to  an 
accompanying  art?iritis  nodosa.  In  the  later  stages  of  the  disease  tran- 
sitory or  permanent  elevations  of  temperature  may  occur,  which  are, 
perhaps,  due  to  such  complications  as  diseases  of  the  lungs  or  acute 
bedsores.  No  constant  changes  have  been  found  in  the  urine.  The 
course  of  progressive  muscular  atrophy  is  essentially  chronic,  but  its 
duration  is  ver}'  variable.and  uncertain.  In  twenty-eight  cases  analyzed 
by  Dr.  Roberts  the  mean,  duration  was  thirty-eight  months ;  of  these 
four  recovered  and  their  mean  duration  was  fourteen  months ;  the 
disease  was  arrested  in  thirteen  c-ases  with  a  mean  duration  of  twenty- 
seven  months,  and  the  remaining  eleven  cases  died  with  a  mean  duration 
of  upwards  of  five  years.  The  disease  may  progress  steadily  until 
nearly  all  the  voluntary  muscles  are  implicated,  and  the  unfortunate 
patient  is  reduced  to  such  utter  helplessness  that  he  is  quite  unable  to 
feed  himself  or  turn  in  bed.  The  advance  of  the  disease  is,  however, 
seldom  continuous,  even  when  it  is  progressive.  Its  course  is  often 
interrupted  by  remissions  which  may  last  for  weeks,  months,  or  even 
years,  or  its  progress  may  be  permanently  arrested  after  some  groups  of 
muscles  have  been  irretrievably  destroyed.  In  a  few  cases  the  atrophied 
muscles  may  be  restored  by  treatment  to  tlieir  former  volume. 

6.  Primary  Labio-glosso-laryngeal  Paralysis  (Chronic 
Progressive  Bulbar  Paralysis  (Wachsmuth)). 

Etiology. — It  does  not  appear  that  heredity  exercises  much  influence 
in  the  production  of  labio-glosso-laryngeal  paralysis.  The  disease 
occurs  most  frequently  between  the  ages  of  forty  and  seventy  years, 
although  it  occasionally  attacks  younger  people.  The  cases  described 
as  occurring  in  children  are  probably  examples  of  insular  sclerosis  in 
which  the  first  diseased  patches  are  localized  on  a  level  with  the  bulbar 
nuclei  and  nerves.  The  disease  attacks  men  twice  as  frequently  as 
women,  and  all  ranks  of  society  appear  to  be  equally  liable  to  it. 

The  exciting  causes  of  progressive  bulbar  paralysis  are  exposure  to  cold, 
blows  on  the  back  of  the  neck,  emotional  excitement,  excessive  mental 
activity,  straining  of  the  affected  muscles  in  singing  and  speaking,  and 
bad  and  insufficient  food.     Syphilis  is  a  frequent  cause  of  the  disease. 

Symptoms. — The  disease  is  generally  preceded  by  slight  premonitory 
symptoms,  such  as  pain  in  the  head  and  back  of  the  neck,  slight  dizzi- 
ness, and  great  diminution  or  complete  loss  of  the  reflex  irritability  of 
the  larynx,  oesophagus,  and  phar^mx. 

The  symptoms  of  chronic  progressive  bulbar  paralysis  begin  stealthily 


SPINAL    ATROPHIC    PARALYSES.  448 

and  creep  on  gradually.  A  slight  affection  of  speech  is  usually  the 
first  symptom  to  attract  attention,  articulation  becomes  indistinct,  and 
the  pronunciation  of  certain  letters  presents  special  difficulty,  while  the 
tongue  and  lips  are  soon  fatigued,  so  that  prolonged  reading  aloud  or 
speaking  is  impossible.  The  articulatory  difficulties  are  followed  bv  a 
gradual  weakness  of  the  lips,  and  of  the  palate.  The  expression  of 
the  face  is  altered,  the  voice  becomes  nasal,  and  the  muscles  of  masti- 
cation and  deglutition  are  so  readily  fatigued  that  the  patient  is  soon 
compelled  to  eat  only  pulpy  food,  and  is  unable  to  swallow  much  at  a 
meal. 

The  initial  debility  and  fatigue  of  the  muscles  may  extend  over  a 
period  of  years  before  the  stage  of  distinct  paralysis  is  reached,  but 
when  once  decided  paralysis  is  established  the  disease  assumes  a  more 
progressive  character,  and  advances  steadily  and  surely  to  a  fatal 
termination. 

When  the  tongue  becomes  more  or  less  paralyzed  the  patient  experi- 
ences an  ever-increasing  difficulty  in  pronouncing  the  dental  and  gut- 
tural sounds,  and  inasmuch  as  the  vowel  i  requires  the  greatest  raising 
of  the  tongue  for  its  production,  its  pronunciation  is  the  first  to  suffer, 
and  then  the  pronunciation  of  the  consonants  r,  s,  ?,  ^,  g,  t,  and  lastly 
d  and  n  become  difficult,  imperfect,  and  finally  impossible.  After  a 
time  the  patient  is  unable  to  effect  the  coarser  and  less  complicated 
lingual  movements.  He  may  at  first  be  able  to  protrude  the  tongue, 
but  not  to  raise  the  tip  towards  the  hard  palate  or  tow-ards  the  nose 
after  protrusion,  while  inability  to  move  the  tip  laterally  indicates  a 
still  greater  degree  of  paralysis.  As  the  paralysis  increases  the  tongue 
cannot  be  lengthened  into  a  point  or  rolled  into  the  form  of  a  tube, 
and  ultimately  the  patient  is  unable  to  protrude  the  organ,  which  now 
lies  behind  the  lower  row  of  teeth  completely  helpless,  and  motionless, 
or  maintained  in  constant  vibration  by  fibrillary  tremors.  The  tongue 
may  maintain  its  normal  aspect,  or  it  becomes  large  and  flabby,  or 
more  frequently  it  is  sodden,  grooved  longitudinally,  wrinkled,  and 
shrunken,  while  simultaneous  atrophy  of  the  papillae  give  a  glazed 
appearance  to  the  surfoce. 

Deglutition  is  rendered  difficult  in  the  early  stages  of  the  disease  by 
the  weakness  of  the  tongue  alone.  The  patient  experiences  a  difficulty 
in  collecting  the  food  so  as  to  form  it  into  a  bolus,  and  in  pressing  it 
back  against  the  soft  palate  and  into  the  pharynx.  In  order  to  over- 
come this  difficulty  the  patient,  after  chewing  his  food  well,  takes  a 
drink  and  throws  his  head  backwards,  while  at  other  times  he  assists 
the  imperfect  movements  of  his  tongue  with  his  fingers,  using  them  to 
extract  the  food  which  has  lodged  between  the  teeth  and  cheeks,  and  to 


444  ATROPHIC    PARALYSES. 

push  the  bohis  to  the  back  of  the  tongue  till  it  is  caught  by  the  retiex 
movements  of  the  pharyngeal  muscles. 

The  glottis  is  not  completely  closed  during  deglutition,  even  at  this 
early  stage,  because  the  root  of  the  tongue  cannot  be  sufficiently  ele- 
vated during;  the  second  stao;e  of  the  act  in  order  to  allow  the  bolus  to 
glide  over  the  depressed  epiglottis.  The  closure  of  the  glottis  is  also 
rendered  still  more  imperfect  by  the  presence  of  paralysis  of  the  muscles 
which  pass  from  the  inferior  maxilla  to  the  hyoid  bone,  a  defect  which  pre- 
vents the  larynx  from  being  raised  as  in  health  during  the  second  stage  of 
deglutition,  and  consequently  the  glottis  fails  to  be  closely  applied  to  the 
epiglottis.  The  imperfect  closure  of  the  glottis  causes  food  and  fluids 
to  find  their  way  into  the  trachea,  and  these  give  rise  to  distressing 
paroxysms  of  cough  and  dyspnoea.  The  saliva  cannot  be  swallowed, 
and  accumulates  in  the  mouth,  and,  owing  to  the  paralysis  of  the 
orbicularis  oris,  flows  from  it  in  a  continuous  stream. 

The  facial  muBcles  are  implicated  soon  after,  or  sometimes  before 
the  muscles  of  the  tongue,  the  orbicularis  oris  being  the  first  to  suffer. 
With  the  increasing  Aveakness  of  the  orbicular  muscle  the  patient  be- 
comes unable  to  Avhistle,  blow,  compress  his  lips,  or  kiss;  he  experi- 
ences difficulty  in  pronouncing  the  vowels  o  and  w,  and  with  the  ad- 
vance of  the  paralysis  the  labial  consonants  p,  /,  i,  and  m  become 
increasingly  difficult  to  articulate. 

Paralysis  of  the  palate  renders  the  formation  of  the  explosive  labial 
consonants  still  more  difficult,  because  the  current  of  air  necessary  to 
force  the  lips  suddenly  asunder  escapes  through  the  nose,  and  the  con- 
sonants p  and  h  are  consequently  turned  into  me  and  ne.  If  the 
patient's  nose  be  closed,  these  letters  are  better  pronounced.  Paralysis  of 
the  palate  also  gives  a  nasal  resonance  to  the  voice,  and  permits  food 
and  fluids  to  escape  readily  through  the  nose  during  efforts  at  degluti- 
tion. When  the  muscles  of  the  tongue,  lips,  and  palate  are  simulta- 
neously paralyzed,  speech  becomes  more  and  more  indistinct,  and  the 
patient  can  only  give  utterance  to  inarticulate  and  grunting  sounds,  but 
the  vowel  a,  being  independent  of  the  articulatory  movements,  can  still 
be  pronounced. 

The  other  facial  muscles  most  liable  to  be  implicated  are  the  quad- 
ratus  and  levator  menti,  the  muscles  of  the  palpebral  and  nasal  regions 
are  never  affected,  and  even  the  elevators  of  the  superior  lips  and  the 
buccinators  are  only  occasionally  paralyzed.  The  paralyzed  muscles 
are  almost  always  distinctly  atrophied,  and  consequently  the  lips  look 
thin,  sharp-edged,  and  furrowed,  and  fibrillary  contractions  are  not 
infrequently  observed  in  them.  The  patient  now  presents  a  very  strik- 
ing and  characteristic  appearance.  The  lower  lip  hangs  loose  and 
pendulous,  the  mouth  is  somcAvhat  increased  in  breadth  and  cannot  be 


SPIXAL    ATliOPHIC    PARALYSES.  445 

closed,  and  tlio  naso-labial  folds  become  deepened  and  give  to  the 
patient  a  laclin-mose  expression.  During  states  of  emotional  excite- 
ment the  lower  part  of  the  face  remains  comparatively  motionless,  and 
contrasts  strongly  -with  the  vivacious  movements  of  the  upper  half  of 
the  face,  and  with  the  brightness  and  activity  of  the  eyes. 

The  saliva  now  flows  from  the  mouth  in  a  continuous  stream  and 
causes  much  annoyance  to  the  patient,  inasmuch  as  it  soaks  through  the 
pillow  at  niglit,  and  requires  to  be  constantly  wiped  from  the  lips  with 
a  handkert-hief  during  the  day.  The  saliva  is  sometimes  unchanged  in 
quality,  while  at  other  times  it  becomes  so  viscid  that  it  may  be  drawn 
out  of  the  mouth  in  long  ropes.  It  appears  to  be  generally  secreted  in 
normal  quantity,  but  sometimes  it  is  increased  to  six  or  eight  times  the 
(juantity  secreted  in  healthy  persons. 

Mastication  is  indirectly  impaired  from  paralysis  of  the  tongue  and 
facial  muscles,  but  after  a  time  it  becomes  still  further  interfered  with 
by  direct  implication  of  the  masticatory  muscles.  The  pterygoid 
muscles  are  the  first  of  the  masticatory  muscles  to  be  attacked,  and  Avith 
paralysis  of  these  the  power  of  effecting  the  lateral  movements  of  the 
lower  jaw  is  lost,  and  with  the  progressive  feebleness  of  the  remaining 
muscles  of  mastication  the  power  of  chewing  the  food  becomes  increas- 
ingly difficult,  feeble,  and  finally  impossible. 

^\\e pharyngeal  muscles  are  now  invaded  and  portions  of  food  lodging 
in  the  pharynx  increase  the  risk  of  foreign  particles  entering  the  larynx, 
Avhile  at  other  times  the  whole  bolus  sets  impacted  on  a  level  with  the 
glottis  and  causes  imminent  danger  of  suffocation. 

The  constrictors  of  the  glottis  are  paralyzed  soon  after  or  simul- 
taneously with  the  pharyngeal  muscles,  and  the  danger  of  swallowing 
either  solids  or  fluids  is  now  much  intensified,  and  solid  particles  freely 
entering  the  trachea  not  only  cause  distressing  paroxysms  of  cough  and 
dyspnoea,  but  are  also  apt  to  pass  into  the  bronchi  and  give  rise  to  a 
fatal  pneumonia. 

The  oesophagus  becomes  ultimately  paralyzed  if  the  patient  survive 
so  long  ;  the  power  of  deglutition  is  now  completely  lost,  and  the  patient 
must  starve  unless  he  is  fed  with  the  stomach  pumj). 

The  laryngeal  muscles  are  sometimes  found  paralyzed  :  the  laryngo- 
scope reveals  paresis  or  paralysis  of  the  vocal  cords,  and  the  voice 
becomes  hoarse  and  feeble,  until  finally  there  is  complete  aphonia. 

The  circulation  is  variously  affected  according  to  the  stage  of  the 
disease.  There  is  no  trustworthy  record  of  retardation  of  the  pulse 
which  could  with  probability  be  referred  to  irritation  of  the  vagus,  but 
a  pulse  rising  before  death  to  from  130  to  150  per  minute,  or  even 
higher,  has  been  frequently  recorded,  and  is  prol)ably  caused  by  paralysis 


446  ATROPHIC    PARALYSES. 

of  the  vagus.  In  the  terminal  period  of  the  disease  patients  often  suffer 
from  fainting  fits,  accompanied  by  great  anxiety  and  a  sensation  of 
impending  death,  and,  indeed,  death  may  result  from  an  attack  of  syncope. 
These  phenomena  are  probably  caused  by  disease  of  the  cardiac  centres 
of  innervation. 

When  the  respiratory  mechanism  is  affected  a  fatal  termination  is 
near.  The  respiratory  movements  become  feeble,  and  owing  to  the  im- 
plication of  the  spinal  accessory  nerves  the  auxiliary  muscles  of  res- 
piration are  paralyzed,  and  superior  thoracic  breathing  is  impossible. 
The  inefficiency  of  the  respiratory  movements  renders  the  breathing 
shallow,  and  all  attempts  at  coughing  or  blowing  the  nose  are  weak  and 
powerless.  After  a  time  the  pneumogastric  nuclei  are  invaded,  and 
spontaneous  paroxysms  of  dyspnoea  with  a  tendency  to  syncope  super- 
vene. The  attacks  of  dyspnoea  become  more  and  more  frequent  as  the 
disease  advances,  while  the  breathing  power  becomes  feebler  and  feebler 
until  ultimately  the  patient  dies  from  asphyxia.  But  the  patient  often 
dies  before  this  advanced  period  of  the  disease  is  reached,  the  fatal  issue 
being  generally  caused  by  an  attack  of  bronchial  catarrh  or  of  pneu- 
monia. 

Atrophy  of  the  paralyzed  muscles  is  usually  most  marked  in  the 
tongue  and  lips,  these  parts  being  likewise  kept  in  constant  movement 
by  fibrillary  contractions.  The  apparent  loss  of  volume  and  the  degree 
of  paralysis  do  not  always  run  a  parallel  course,  and  the  tongue  some- 
times retains  its  normal  volume  while  completely  paralyzed,  but  a  sub- 
sequent microscopical  examination  will  show  that  the  muscular  fibres 
have  undergone  extensive  degeneration. 

The  electrical  excitability  is  said  by  most  authors  not  to  undergo  any 
noteworthy  changes,  but  Erb  states  that  he  lias  met  with  the  most  marked 
"reaction  of  degeneration"  on  direct  irritation  of  the  muscles  of  the 
chin,  lips,  and  tongue.  The  electrical  irritability  of  the  nerves  was 
normal  or  but  slightly  diminished. 

The  sensibility  generally  remains  unaffected  throughout  the  whole 
course  of  the  disease.  Buzzing  in  the  ears  and  deafness  have  occasionally 
been  present,  and  in  some  cases  various  parsesthesijB,  or  even  a  consider- 
able degree  of  anaesthesia  of  one  or  both  sides  of  the  face,  loss  of 
common  sensation  on  the  tongue,  and  pain  in  the  occipital  and  upper 
cervical  regions  have  been  observed. 

The  intelligence  remains  quite  clear  to  the  last,  but  the  temper  is 
somewhat  excitable,  and  patients  often  manifest  an  inclination  to  laugh 
or  weep  on  slight  provocation. 

Reflex  irritability  is  often  much  diminished  or  lost  in  the  tongue,  soft 
palate,  pharynx,  and  even  in  the  larynx  before  the  appearance  of  any 


SPINAL    ATROPHIC    PARALYSES.  447 

Other  symptom,  but  it  is  sometimes  retained  in  these  parts  until  a  late 
period  of  the  disease. 

Vaso-motor  disturbances  have  not  been  recorded,  and  there  is  no 
fever  during  the  whole  course  of  the  disease. 

G-eneral  nutritive  disorders  occur  sooner  or  later  in  the  course  of  this 
disease,  owing  in  great  part  to  the  insufficient  quantity  of  food  which  the 
patient  is  able  to  take.  The  patient  becomes  after  a  time  greatly  ema- 
ciated, and,  unable  to  get  up,  he  sits  in  bed  with  the  upper  part  of  the 
body  propped  up,  and  with  the  head  resting  on  pillows  and  inclined  to 
one  side  in  order  to  let  the  saliva  flow  out  of  the  mouth.  When  this 
condition  is  reached  death  soon  supervenes,  either  from  a  paroxysm  of 
dyspnoea,  or  suddenly  and  quietly  from  arrest  of  the  heart's  action. 

The  course  of  this  form  of  bulbar  paralysis  is  always  slow  and  chronic, 
but  surely  progressive.  There  is  seldom  a  remission  of  long  duration 
and  recovery  has  never  been  observed  Avhen  the  diagnosis  of  the  primary 
disease  was  beyond  question.  The  disease  is  usually  fatal  in  from  one 
to  five  years. 

Complications. — Progressive  muscular  atrophy  is  the  most  important 
and  frequent  complication  of  bulbar  paralysis,  the  latter  disease  being 
sometimes  the  primary  afiection,  and  at  other  times  a  terminal  phenome- 
non supervening  in  the  course  of  the  former.  The  two  affections  are, 
indeed,  essentially  the  same  disease,  both  as  regards  the  clinical  symp- 
toms and  the  anatomical  changes  formed  after  death. 

Amyotrophic  lateral  sclerosis  is  another  important  complication  of 
progressive  bulbar  paralysis.  In  the  cases  which  concern  us  at  present 
the  phenomena  of  bulbar  paralysis  are  primary,  but  in  the  course  of  the 
disease  the  lower  extremities  become  the  subjects  of  a  gradually  increas- 
ing paralysis  which  is  characterized  by  the  muscular  tension,  and  ex- 
ag-gerated  tendon-reactions  which  are  held  to  indicate  disease  of  the 
lateral  column  of  the  cord. 


7.  Ophthalmoplegia  Externa  vel  Progressiva. 

Etiology. — The  two  known  causes  of  the  disease  are  syphilis  and 
rheumatism. 

Symptoms. — The  first  symptom  to  attract  attention  is  usually  a 
drooping  of  the  eyelids,  which  gives  to  the  patient  a  peculiar  sleepy 
appearance.  Soon  afterwards  all  the  muscles  of  the  eyeballs  manifest 
signs  of  weakness,  the  aff"ection  is  usually  bilateral,  and  every  possible 
combination  of  paralysis  may  occur,  but  the  muscles  are  always  attacked 
in  groups  and  not  singly.     The  pupils  are  in  a  medium  state  of  dilata- 


448  ATROPHIC    PARALYSES. 

tion,  and  their  reflex  contraction  to  light  is  either  sluggish  or  lost.  The 
condition  of  accommodation  has  not  always  been  tested,  but  in  some 
cases  it  was  found  normal.  White  atrophy  of  the  optic  disks,  with 
blindness,  was  present  in  one-third  of  the  cases  reported  by  Hutchinson. 
In  some  cases  the  fifth  nerves,  and  in  others  the  facial  nerves  were 
involved  in  the  disease,  while  in  one  case  reported  by  Hutchinson  the 
palate  was  affected  and  smell  was  lost.  In  some  of  the  recorded  cases 
the  patellar  tendon-reaction  was  absent,  and  other  symptoms  indicative 
of  locomotor  ataxia  were  present.  It  seems,  indeed,  likely  that  a  con- 
siderable number  of  the  reported  cases  Avere  examples  of  locomotor 
ataxia  in  which  the  ocular  troubles  were  unusually  well  marked. 


Y.  MYOPATHIC  ATROPHIC  PAPvALYSES. 
PSEUDO-HYPERTIIOPHIC    PARALYSIS    AND    Erb'S    JuVENILE    FoRM    OF 

Progressive  Muscular  Atrophy. 

Etiology. — Pseudo-hypertrophic  paralysis  was  supposed  to  begin 
almost  always  in  infancy,  but  if  we  include  Erb's  juvenile  form  of 
muscular  atrophy,  it  will  be  seen  that  adults  are  frequently  attacked, 
although  in  these  cases  the  symptoms  make  their  appearance  between 
five  and  thirteen  years  of  age.  The  disease  is  much  more  common  in 
boys  than  in  girls ;  out  of  two  hundred  and  twenty  cases  collected  by 
Gowers  one  hundred  and  ninety  Avere  boys  and  thirty  girls.  Hereditary 
predisposition  to  the  disease  can  often  be  traced.  Two  children  in  the 
same  family  are  often  attacked,  and  Meryon  met  with  a  family  in  which 
eight  children  were  the  subjects  of  the  disease,  while  other  equally 
striking  examples  have  been  reported  by  others.  It  is  very  probable 
that  all  the  cases  of  supposed  progressive  muscular  atrophy  in  which 
numerous  members  of  the  same  family  were  attacked,  such  as  the  cases 
reported  by  Hemptenmacher,  Friedreich,  Hammond,  and  Naunyn,  really 
belong  to  Erb's  juvenile  paralysis,  and  Avill  therefore  have  to  be  trans- 
ferred to  this  group.  A  remarkable  circumstance  about  the  heredity 
of  this  disease  is  that  it  is  mainly  confined  to  the  male  sex,  yet  the 
descent,  so  far  as  is  known,  is  always  through  the  mother's  side.  The 
disease  is  not,  as  a  rule,  transmitted  directly  from  parent  to  offspring, 
inasmuch  as  the  majority  of  its  victims  are  attacked  at  an  early  age, 
and  they  do  not,  therefore,  become  parents.  For  the  same  reason  the 
disease  cannot  be  regarded  as  an  example  of  atonism.  It  must,  there- 
fore, be  inferred  that  a  certain  predisposition  is  transmitted  which,  with 
the  concurrence  of  other  unfavorable  circumstances,  such  as  an  eruptive 
fever,  develops  the  disease. 


MYOPATHIC    ATROPHIC    PARALYSES.  449 

The  exciting  causes  of  the  disease  are  not  well  known.  Exposure 
to  cold  and  damp  appears  to  be  occasionally  the  determining  cause, 
while  at  other  times  it  has  followed  an  eruptive  fever,  variola,  or 
measles,  and  several  cases  have  been  ushered  in  by  convulsions. 

Symptoms. — When  pseudo-hypertrophic  paralysis  begins  in  infancy 
the  parents  do  not  notice  that  anything  is  wrong  until  the  child  arrives 
at  the  age  when  he  ought  to  begin  to  walk.  At  this  period  it  is  noticed 
that  when  the  child  is  placed  on  his  feet  he  does  not  instinctively  move 
his  legs  to  walk,  but  they  double  helplessly  under  him,  or  the  child 
may  have  begun  to  walk,  but  it  is  observed  that  he  is  soon  fatigued, 
and  that  he  is  unable  to  stand  steadily  or  walk  without  stumblino-. 
The  parents  are  not  readily  alarmed  at  the  inability  of  the  child  to 
walk,  because  the  lower  limbs  appear  to  be  unusually  well  developed. 

The  appearance  of  muscular  strength  is  caused  by  an  increase  in 
volume  of  some  of  the  muscles,  but  this  increase  is  due,  as  we  shall 
hereafter  see,  to  morbid  changes  occurring  chiefly  in  the  connective 
tissue  of  the  muscle,  and  which  are  always  attended  by  a  diminution  of 
its  power.  The  apparent  hypertrophy  of  the  muscles  generally  begins 
by  enlargement  of  one  calf,  the  other  soon  becoming  affected.  The 
gluteal  muscles  are  soon  invaded,  and  then  the  disease  successively 
attacks  the  lumbo-spinal  muscles,  the  muscles  of  the  thigh,  trunk, 
shoulders,  and  upper  arms,  while  the  muscles  of  the  neck,  face,  tongue, 
forearms,  or  hands  may  occasionally  be  attacked,  but  only,  as  a  rule,  at 
a  late  period  of  the  disease.  The  aftected  muscles  may  attain  an 
enormous  volume,  and  stand  out  so  prominently  under  the  skin  that 
Duchenne  uses  the  term  "hernial  protrusions"  to  describe  their  ap- 
pearance. The  muscles  feel  hard  and  resisting  to  the  touch,  so  that  the 
whole  appearance  of  the  patient  often  suggests  the  idea  of  Herculean 
strength  instead  of  the  great  feebleness  Avhich  really  exists.  But  even 
in  the  midst  of  all  this  apparent  development  of  muscular  power  there 
are  not  wanting  visible  indications  of  the  real  nature  of  the  malady, 
inasmuch  as  some  of  the  muscles  are  always  found  atrophied  and  their 
wasted  condition  contrasts  strongly  with  the  excessive  size  of  the  others. 
In  the  majority  of  cases  the  gastrocnemii  and  the  gluteal  muscles  are 
increased  in  size,  while  those  of  the  thigh  often  undergo  some  degree  of 
atrophy,  and  consequently  the  slender  thighs  afford  a  marked  contrast 
to  the  enlarged  calves  and  buttocks.  In  the  upper  part  of  the  body 
the  atrophy  frequently  predominates.  The  deltoids  are  usually  enlai-ged, 
but  the  remaining  muscles  of  the  arm  and  the  pectoral  muscles  undergo 
atrophy,  while  those  of  the  forearm  and  hand  are  often  spared  until  a 
late  period  of  the  disease.  Of  the  muscles  which  move  the  shoulder 
the  rhomboids  and  the  serrati  are  the  most  liable  to  be  :itt:icked,  and 

29 


450  ATROPHIC    PARALYSES. 

these  are  generally  atrophied  instead  of  being  enlarged.  In  a  large 
majority  of  cases,  therefore,  the  uj^per  part  of  the  body  is  contrasted  by 
its  slenderness  with  the  unusual  development  of  the  lower  extremities, 
and  perhaps  the  greatest  contrast  is  afforded  by  the  thin  arm,  which 
often  consists  of  scarcely  anything  more  than  the  humerus  surrounded 
by  skin,  and  the  normal  condition  of  the  forearm  on  the  one  hand,  with 
the  prominence  of  the  enlarged  deltoid  on  the  other. 

The  relative  distribution  of  the  hypertrophied  and  atrophied  muscles 
just  described  is  that  usually  met  with  in  the  cases  named  by  Erb  "the 
juvenile  form  of  progressive  muscular  atrophy,"  but  I  can  see  no 
essential  difference  between  these  cases  and  those  in  which  the  muscular 
hypertrophy  is  more  widely  distributed.  Pseudo-hypertrophy  of  muscles 
does  not,  indeed,  appear  to  be  a  necessary  part  of  the  diseases  Avhich 
mav  be  grouped  together  as  myopathic  atrophic  paralyses.  In  the  cases 
described  by  Leyden  under  the  name  of  "  hereditary  muscular  atrophy,"' 
the  slight  degree  of  increase  of  volume  observed  in  some  of  the  muscles 
is  quite  subordinate  to  the  widely  diffused  atrophy  of  others.  Cases 
have  been  described  by  Zimmerlin  which  appear  to  belong  to  the  myo- 
pathic atrophic  paralyses,  and  in  which  the  muscles  of  the  shoulders 
and  arms  were  atrophied  without  any  admixture  of  pseudo-hypertrophy, 
and  cases  have  been  described  by  Landouzy  and  Dejerine  which  must 
also  apparently  be  included  in  this  category,  and  in  which  the  symptoms 
began  in  infancy  by  atrophy  of  the  muscles  of  the  face,  the  muscles  of 
the  shoulders  and  arms  being  invaded  about  the  age  of  eleven  years. 
In  short,  the  group  of  myopathic  atrophic  paralyses  presents  several 
varieties,  but  we  shall  at  present  proceed  with  the  more  usual  form  of 
the  disease  as  represented  by  the  affection  known  under  the  name  of 
pseudo-hypertrophic  paralysis. 

The  relative  degree  of  paralysis  of  groups  of  muscles  gives  rise  as 
usual  to  certain  deformities,  and  one  of  the  most  notable  of  these  occurs 
in  the  foot.  The  gastrocnemius  muscle  undergoes  progressive  shorten- 
ing, partly  perhaps  owing  to  the  internal  changes  it  is  undergoing,  and 
partly  owing  to  the  increasing  paralysis  of  the  anterior  muscles  of  the 
foot.  But  whatever  may  be  the  cause,  the  result  of  this  shortening  is 
that  the  patient  experiences  difficulty  in  bringing  the  heel  to  the  ground, 
and  as  the  disease  advances  a  permanent  condition  of  talipes  ecjuinus 
or  equino-varus  is  established.  The  foot  also  becomes  more  hollow  and 
the  plantar  arch  increased,  while  paralysis  of  the  interossei  causes  the 
first  phalanges  to  be  maintained  in  a  state  of  exaggerated  extension  on 
the  metatarsal  bones,  and  the  distal  phalanges  to  be  flexed,  so  that  the 
toes  assume  the  peculiar  claw-like  appearance  which  Duchenne  has 
called  griffe  des  orteils.     A  remarkable  curvature  of  the  spine  in  the 


MYOPATHIC    ATROPHIC    PARALYSES.  451 

lumbo-sacral  region,  named  by  Duchenne  lordosis  or  saddle-hack,  is  one 
of  the  most  constant  symptoms  of  the  disease.  This  deformity  is  not 
seen  until  the  patient  stands  or  walks  ;  the  shoulders  and  the  upper  part 
of  the  vertebral  column  are  then  carried  backwards,  so  that  a  plumb- 
line  let  fall  from  the  most  prominent  spinous  process  of  the  vertebral 
column  falls  behind  the  sacrum.  This  deformity  is  produced  by  com- 
parative feebleness  of  the  extensors  of  the  pelvis  and  the  erector  muscles 
of  the  spine.  Weakness  of  the  extensors  allows  the  pelvis,  and  with  it 
the  loAver  vertebra,  to  incline  forwards  when  the  patient  assumes  the 
erect  posture,  and  a  compensatory  backward  inclination  of  the  dorsal 
spine  is  rendered  necessary  in  order  to  keep  the  centre  of  gravity  in  the 
normal  position.  The  posterior  displacement  of  the  upper  part  of  the 
body  also  causes  the  line  of  gravity  to  fall  behind  the  trochanters  of  the 
femur  and  takes  off  all  strain  from  the  enfeebled  erector  muscles  of  the 
spine  and  the  gluteal  muscles.  The  attitude  of  the  patient  on  assum- 
ing the  erect  posture  is  quite  characteristic  of  the  disease.  The  feet 
are  kept  widely  apart,  and  the  patient  cannot  approximate  them  without 
risk  of  falling.  In  the  early  stage  of  the  disease  the  heels  are  brought 
to  the  ground,  but  after  a  time  the  patient  has  to  balance  himself  upon 
his  toes,  and  at  the  same  time  the  dorsal  curve  becomes  very  pronounced, 
and  in  consequence  of  these  deformities  the  power  of  the  patient  to 
maintain  the  erect  posture  becomes  very  precarious  and  the  slightest 
push  suffices  to  throw  him  down. 

The  gait  of  the  patient  is  no  less  characteristic  than  his  attitude  in 
the  erect  posture.  We  have  seen  that  the  feet  are  held  apart,  and  in 
walking  the  body  is  inclined  first  to  one  side  then  to  the  other,  so 
that  the  gait  resembles  the  Avaddling  of  a  duck.  When  the  feet  are 
kept  widely  apart  the  centre  of  gravity  must  be  carried  at  each  step 
well  over  to  the  side  of  the  active  leg,  in  order  that  the  line  of  gravity 
may  pass  through  the  centre  of  the  arch  of  the  foot  planted  on  the 
ground.  Duchenne  thought  that  the  oscillation  of  the  body  in  walking 
was  an  instinctive  movement  on  the  part  of  the  patient  in  order  to  avoid 
putting  a  strain  upon  the  paralyzed  gluteus  medius.  But  in  a  case  of 
muscular  atrophy  observed  by  myself  the  gluteus  medius  was  completely 
paralyzed  on  each  side,  yet  instead  of  the  waddling  gait  so  characteristic 
of  pseudo-hypertrophic  paralysis,  the  head  and  body  were  moved  for- 
Avards  during  locomotion  almost  in  a  straight  line,  and  without  the 
lateral  inclinations  being  at  all  equal  to  those  observed  in  healthy  per- 
sons. From  an  examination  of  several  cases  of  this  disease  it  appears 
to  me  that  the  lateral  inclinations,  instead  of  being  caused  by  paralysis 
of  the  gluteus  medius,  are  mainly  effected  by  alternate  contractions  of 
these  muscles,  and  are  rendered  necessary  partly  by  the  legs  being  held 


452  ATEOPHIC    PAEALYSES. 

widely  apart,  and  partly  by  the  inability  of  the  patient  to  clear  the  toes 
of  the  advancing  foot  from  the  ground  by  producing  dorsal  flexion  of 
the  foot.  As  the  disease  advances  the  patient,  as  we  have  seen,  becomes 
unable  to  bring  the  heel  to  the  ground,  and  at  each  step  the  body  must 
be  delicately  balanced  in  order  that  the  line  of  gravity  may  pass  through 
or  a  little  behind  the  ball  of  the  active  foot,  and  the  slightest  displace- 
ment of  the  centre  of  gravity  will  cause  the  patient  to  fall.  It  is, 
therefore,  necessary  that  at  each  step  the  body  should  be  inclined  well 
over  to  the  side  of  the  active  leg,  and  the  patient  aids  himself  in  main- 
taining the  centre  of  gravity  vertically  above  the  ball  of  the  foot  on  the 
ground  by  moving  his  arms  about  like  a  rope  dancer. 

The  manner  in  which  the  patient  attains  the  erect  posture  is  equally 
characteristic.  When  he  is  laid  down,  or  falls,  he  drags  himself  up 
with  the  aid  of  his  arms  if  a  chair  or  other  article  of  furniture  is 
sufficiently  near  for  him  to  lay  hold  of.  But  when  he  has  to  get  uj) 
without  extraneous  aid,  the  body  is  first  raised  on  the  hands  and  feet. 
In  this  attitude  the  feet  are  planted  on  the  ground,  the  different  seg- 
ments of  the  lower  extremities  are  slightly  flexed  upon  one  another, 
the  body  is  flexed  on  the  lower  extremities,  and  more  or  less  horizontal, 
the  head  is  directed  downwards,  and  the  tips  of  the  fingers  of  both 
hands  rest  on  the  ground  in  front  of  the  toes.  The  patient  next  raises 
his  hand,  say  the  left,  and  places  it  above  the  left  knee.  The  body  is 
now  drawn  over  to  the  opposite  side  so  that  its  weiglit  rests  mainh^  on 
the  right  leg,  and  by  one  vigorous  push  of  the  left  arm  the  left  knee  is 
thrust  backwards,  and  the  leg  and  thigh  are  thus  extended  upon  one 
another,  while  the  body  is  at  the  same  time  thrust  upwar<ls.  Simulta- 
neously with  this  action  the  weight  of  the  body  is  transferred  from  the 
right  to  the  left  leg,  and  the  right  hand  is  elevated  and  planted  above 
the  knee  on  the  corresponding  side,  and  a  backward  push  on  that  knee 
causes  the  different  segments  of  that  limb  also  to  become  extended  upon 
one  another.  The  patient  has  now  attained  the  second  posture,  and  in 
this  position  his  feet  are  planted  on  the  ground,  the  lower  extremities 
are  directed  upwards  or  backwards,  and  the  body  is  inclined  upwards 
while  the  arms  prop  up  the  trunk  by  passing  from  it  to  the  knees 
where  the  hands  are  placed.  The  fact  that  the  weight  of  the  upper 
part  of  the  trunk  is  directed  through  the  arms  to  the  knees  redis- 
tributes the  force  in  such  a  way  that  the  knees  are  pushed  backwards, 
and  thus  the  thighs  and  legs  tend  to  become  extended  upon  one  another, 
the  heels  are  forced  downwards,  and  so  the  patient  is  fixed  firmly  to  the 
ground,  and  the  trunk  is  maintained  in  its  upward  and  forward  attitude 
without  any  strain  being  placed  upon  the  enfeebled  extensors  of  the 
body.     The  next  great  effort  of  the  patient  is  directed  to  attain  the 


MYOPATHIC    ATROPHIC    PARALYSES.  453 

erect  posture,  and  in  accomplishing  this  object  it  is  said  that  he  thrusts 
his  body  upwards  by  gradually  chmbing  up  his  thighs.  This  de- 
scription is  very  graphic,  but  it  is  only  partially  accurate.  The 
movement  by  which  the  pelvis  is  elevated  upon  the  thighs  is,  indeed,  a 
very  complicated  one,  and  is  effected  not  by  simple  extension,  but  bv  a 
kind  of  screw  movement. 

The  patient  experiences  great  difficulty  in  getting  up  steps,  owino-  to 
the  feebleness  of  the  gluteus  maximus.  He  lays  hold  of  the  railing  with 
one  hand,  say  the  right,  and  drags  his  body  upwards  at  each  step. 
The  right  arm  is,  however,  assisted  by  the  left.  The  left  hand  is 
planted  above  the  knee  upon  the  same  side,  and  each  time  the  left  leg  is 
raised  a  step  the  body  is  thrust  upwards  by  the  various  segments  of 
the  left  arm  being  extended  upon  one  another.  The  disease  now  be- 
comes stationary  for  two  or  three  years,  and  sometimes  for  a  much 
longer  period,  and  as  the  general  health  is  good  and  the  muscular 
development  apparently  very  powerful,  the  parents  cannot  believe  that 
the  affection  is  incurable.  This  illusion  is,  however,  after  a  time  des- 
tined to  be  dispelled.  The  feebleness  of  the  lower  extremities  gradu- 
ally increases,  so  that  the  child  cannot  maintain  the  erect  posture, 
while  the  muscles  of  the  superior  extremities  also  become  both  para- 
lyzed and  atrophied,  and  even  the  hypertrophied  limbs  begin  to  waste. 
The  patient,  now  arrived  at  adolescence,  may  live  on  for  several  years 
in  a  condition  of  almost  complete  paralysis,  until  finally  death  takes 
place  from  exhaustion,  implication  of  the  respiratory  muscles,  or,  more 
usually,  from  some  intercurrent  affection. 

The  patellar  tendon-reaction  is  lost  at  a  comparatively  early  period 
of  the  disease,  and  the  electrical  reaction  of  the  muscles  remains  normal 
so  long  as  any  muscular  fibre  is  left.  The  skin  over  the  affected  parts 
often  presents  a  mottled  appearance,  and  the  superficial  temperature  of 
the  inferior  extemities  has  sometimes  been  found  higher  than  that  of 
the  trunk. 

The  disease  is  associated  with  a  certain  amount  of  mental  incapacity. 
Patients  are  sometimes  slow  in  acquiring  speech,  others  are  obtuse  in 
intelligence,  and  some  are  idiots.  The  disease  is  unaccompanied  by 
suffering,  there  is  no  alteration  of  sensibility,  and  the  functions  of  the 
bladder  and  rectum  are  unaffected,  while  the  general  health  is  not  in- 
terfered with  until  the  terminal  period  of  the  disease. 

The  course  of  the  disease  is  always  chronic.  It  begins  insidiously, 
and  consists  of  a  first  stage,  in  which  there  is  progressive  enfeeblement 
of  the  lower  extremities,  saddle-back,  and  waddling  gait,  and  which 
may  last  from  a  few  weeks  to  some  years  before  the  commencement  of 
the  next  stage.    This  second  period  is  characterized  by  apparent  hyper- 


454  ATROPHIC    PARALYSES. 

trophy  of  a  certain  number  of  muscles  usually  beginning  in  those  of 
the  calf,  and  extending  gradually  to  other  muscles  of  the  trunk  and 
upper  extremities.  The  stage  of  hypertrophy  attains  its  maximum 
extent  and  intensity  generally  eighteen  months  from  the  beginning  of 
the  second  stage.  The  symptoms  now  remain  stationary  for  two  or 
three  or  for  many  years.  Some  of  the  cases  described  by  Erb  under 
the  name  of  "the  juvenile  form  of  progressive  muscular  atrophy,"  live 
to  a  moderately  old  age,  and  the  disease  may  then  remain  more  or  less 
stationary  for  from  ten  to  twenty  or  more  years. 

The  third  stage  of  the  disease  is  now  ushered  in  by  a  still  furtlier 
enfeeblement  of  the  affected  muscles,  and  by  the  extension  of  the  paral- 
ysis to  the  superior  extremities.  Abduction  and  elevation  of  the  arm  are 
at  first  rendered  difficult,  and  by  and  by  the  paralysis  gradually  impli- 
cates the  other  movements  of  the  arm. 

The  last  stage  of  the  disease  generally  begins  about  puberty,  although 
it  is  sometimes  deferred  until  a  moderately  mature  age.  The  slight 
power  of  movement  of  which  the  patient  was  capable  becomes  gradually 
lost,  so  that  he  can  only  sit  in  a  chair  or  recline  on  a  couch.  The 
patient  may  continue  to  live  for  a  long  time  in  this  condition,  but 
eventually  death  supervenes  from  exhaustion  or  some  intercurrent 
malady. 

Morbid  Anatomy  and  Physiology  of  the  Atrophic  Paralyses. 

1.  Changes  in  the  Nervous  System. — Paralysis  of  the  muscles  sup- 
plied by  individual  nerves  is  caused  by  a  local  neuritis,  by  injuries  of 
the  nerve  from  external  wounds,  or  by  compression  of  it  from  tumors 
growing  in  the  nerve  or  in  neighboring  structures.  When  a  nerve  is 
seriously  injured  in  any  part  of  its  course,  the  peripheral  part  under- 
goes the  Wallerian  degeneration,  and  the  muscles  supplied  by  it  are  not 
only  paralyzed,  but  also  undergo  atrophy. 

The  morbid  anatomy  of  progressive  multiple  neuritis  has  already 
been  described.  The  most  important  changes  observed  in  lead  paral- 
ysis have  been  found  in  the  intramuscular  nerve  fibres,  and  in  the 
musculo-spiral  nerve.  The  connective  tissue  and  the  sheath  of  the 
primitive  fibres  are  thickened,  while  the  axis-cylinders  are  sometimes 
distinctly  visible,  and  at  other  times  disappear  altogether.  Vitreous 
degeneration  and  atrophy  of  the  ganglion  cells  have  been  found  by 
some  observers,  while  others  failed  to  detect  any  change  in  the  spinal 
cord. 

In  diphtheritic  paralysis  the  nerves  of  the  palate  have  been  found 
altered  in  the  same  manner  as  occurs  in  the  peripheral  end  of  a  nerve 


MYOPATHIC    ATROPHIC    PARALYSES, 


-i55 


after  section,  and  Dejerine  found  similar  alterations  in  the  anterior  roots 
of  the  nerves  on  a  level  with  that  portion  of  the  spinal  cord  from  which 
the  paralyzed  muscles  are  innervated.  Changes  have  also  been  ob- 
served in  the  anterior  gray  horns  of  the  spinal  cord,  but  they  are 
slight,  and  the  balance  of  evidence  appears  to  favor  the  idea  that  the 
primary  lesion  is  situated  in  the  course  of  the  nerves.  In  alcoholic 
paralysis  also  the  most  recent  observations  seem  to  prove  that  the  paral- 
ysis is  caused  by  a  neuritis  of  the  peripheral  nerves.  No  anatomical 
changes  have  as  yet  been  discovered  in  those  cases  of  reflex  paralysis 
which  are  attended  with  w'asting  of  the  extensor  muscles  of  the  in- 
flamed joint. 

In  the  spinal  atrophic  paralyses  the  chief  lesions  have  been  found  in 
the  anterior  gray  horns  of  the  spinal  cord. 

In  acute  ascending  paralysis  post-mortem  examinations  have  yielded, 
for  the  most  part,  completely  negative  results,  no  morbid  changes 
whatever  having  been  detected  in  the  spinal  cord,  peripheral  nerves,  or 


Fig.  139. 


The  letters  o,  h,  c  indicate  respectively  tlie  central,  antero-lateral,  and  postevo-Iateral  groups  of  ganglion 
cells  On  the  left  side  the  group  h  has  almost  entirely  disappeared,  causing  a  marked  falling  in  of  the 
circumference  of  the  gray  matter.  The  groups  a  and  c  are  fairly  well  represented  on  the  left  side,  but  the 
cells  composing  them  are  not  so  numerous  as  on  the  right.  The  internal  group  lias  disappeared  from  l.iotli 
sides.     (After  Humphreys.) 

muscles.  In  other  recorded  cases,  which  apparently  were  examples  of 
the  disease,  the  usual  signs  of  an  acute  myelitis  were  discovered,  while 
in  a  case  reported  by  Dejerine  and  Goltz  decided  evidences  of  a  degen- 
erative neuritis  were  found  in  the  anterior  roots  of  the  spinal  nerves. 
It  is  very  probable  that  some  of  the  cases  recorded  as  examples  of 
Landry's  paralysis  really  belong  to  the  group  of  progressive  multiple 
neuritis. 


4:66 


ATROPHIC    PARALYSES. 


Acute  spinal  atrophic  jjaralt/sis  appears  to  be  an  acute  inflammation 
which  remains  more  or  less  limited  to  the  anterior  gray  horns  of  the 
spinal  cord  (Fig.  139).  The  antero-lateral  columns  may  also  manifest 
a  greater  or  less  degree  of  sclerosis,  while  the  anterior  roots  and  the 
efferent  fibres  of  the  peripheral  nerves  give  evidence  of  having  under- 
gone a  degenerative  atrophy.  In  old-standing  cases  the  anterior  horn 
of  the  affected  side,  when  the  disease  is  unilateral,  undergoes  marked 
atrophy  as  compared  with  the  healthy  one  (Fig.  140). 

Fig.  140. 


Tr.insverse  Section  of  the  Spinal  Cord 
taken  from  the  cervical  region  of  a  woman,  aged  fifty  years,  who  died  in  the  Salpetritre,  of  general  paral- 
ysis of  the  insane,  and  who  was  the  subject  ot  infantile  spinal  paralysis  of  the  right  superior  extremity. 
There  was  fibroid  atrophy  of  the  right  anterior  cornu,  and  atrophy  of  all  the  white  columns  of  the  corre- 
sponding side.     (From  Charcot.) 


In  eli7'onic  atrophic  spinal  paralysis  the  post-mortem  examinations 
hitherto  obtained  have  been  few,  but  cases  have  been  recorded  by 
Cornil,  Webber,  Aufrecht,  Dreschfeld,  and  myself.  The  chief  changes 
were  found  in  the  anterior  gray  horns,  and  consisted  in  disappearance 
and  atrophy  of  the  ganglion  cells,  destruction  of  their  processes,  thick- 
ening of  the  walls  of  the  bloodvessels,  and  exudation  of  the  white  and 
of  a  few  red  blood-corpuscles  into  the  perivascular  spaces.  The  case 
recorded  by  myself  was  that  of  a  young  girl  aged  fifteen  years,  who 
had  died  from  respiratory  paralysis  after  having  the  typical  symptoms 
of  the  disease  for  seven  months.  The  ganglion  cells  had  almost  com- 
pletely  disappeared    from    the    anterior   horns   throughout    the  entire 


MYOPATHIC    ATROPHIC    PARALYSES. 


457 


length  of  the  spinal  cord  (Fig.  141,  1  to  4),  while  the  upward  contin- 
uation of  the  anterior  horns  in  the  medulla  was  similarly  affected  but  to 
a  less  degree  (Fig.  141,  5).  Slight  changes  were  observed  in  the  columns 
of  Goll,  which  showed  that  the  lesion  was  not  strictly  limited  to  the 
anterior  horns,  although  they  were  the  portions  which  chiefly  suffered. 


Fig.  141. 


Tkansverse  Sections  of  the  Spinal  Cord  and  JIedulla  Oblongata  at  different  levels,  fuom  a  case 

OF  CHRONIC  atrophic  SPINAL  PARALYSIS,  SHOWING  THE   DISAPPEARANCE  OF  THE  GANGLION  CELLS. 

(Young.) 
1,  Jliddle  of  the  lumbar  enlargement ;  2,  Middle  of  the  dorsal  region  ;  3,  Middle  of  the  cervical  enlarge- 
ment ;  4,  Section  on  a  level  with  the  origin  of  the  second  cervical  nerve ;  5,  Section  of  the  medulla  oblon- 
gata on  a  level  with  the  middle  third  of  the  olivary  body. 


In  'periependymal  myelitis  the  gray  column  which  surrounds  the 
central  canal  is  the  seat  of  inflammatory  changes.  These  changes  con- 
sist in  some  cases  of  a  proliferation  of  the  epithelioid  cells  which  line  the 
central  canal,  while  in  other  cases  the  morbid  process  appears  to  begin 
in  the  neuroglia  which  surrounds  the  canal,  and  the  central  grav  column 
becomes  converted  into  a  solid  mass  of  fibroid  tissue  which  grows  from 
within  outwards,  and  invades  the  remaining  parts  of  the  gray  matter. 
The  central  core  may  be  solid  throughout  the  whole  extent  of  the  cord, 
but  in  most  cases  a  portion  of  the  interior  undergoes  softening  and  a 
cavity  is  formed  which  is  filled  with  serous  fluid.  The  cavity  varies 
greatly  in  its  dimensions ;  it  sometimes  extends  the  whole  length  of  the 
cord,  while  at  other  times  it  is  only  a  few  lines  in  length  ;  and  on  trans- 
verse section  it  is  sometimes  large  enough  to  admit  the  tip  of  the  finger, 
while  at  other  times  it  is  only  large  enough  to  be  visible  to  the  naked 
eye.  The  cavity  is  usually  situated,  not  in  the  position  of  the  central 
canal,  but  in  that  part  of  the  posterior  columns  which  adjoins  the  pos- 
terior commissure,  and  the  central  canal  can  generally  be  found  lying 
in  front  of  it.  The  cavity  is  always  surrounded  by  a  ring  of  fibroid 
tissue,  which  grows  from  within  outwards,  and  invades  the  gray  sub- 


458 


ATROPHIC    PARALYSES. 


Stance  of  the  cord,  and  which  may  even  extend  to  the  white  substance, 
especially  to  the  lateral  columns.  In  some  cases  the  cavity  forms  the 
predominating  feature  of  the  morbid  change,  while  in  others  the  cavity 
is  insignificant  and  almost  the  whole  of  the  central  gray  column  is  con- 
verted into  a  dense  mass  of  sclerosed  tissue.  In  the  annexed  woodcut 
(Fig.  142)  borrowed  from  Leyden,  a  section  of  the  cervical  enlargement 

Fig.  14-2. 


Transverse  Sf.ction  of  the  Spinal  Cord  from  the  Middle  of  the  Cekvical  Enlargement,  from 
A  CASE  OF  Syringomyelia,  showing  a  cavity  behind  the  posTERioa  commissure,  and  destruction  of  a 

LARGE  portion  OF  THE  GANGLION  CELLS  OF  THE  ANTERIOR  GRAY  HORNS.      (FrOIlI  LeYDEN.) 


of  the  spinal  cord,  from  a  case  of  syringomyelia,  is  represented :  the 
central  gray  column  is  changed  into  a  substance  of  a  gelatinous  con- 
sistence, Avhich  became  softened  into  cavities  at  certain  points.  In  a 
case  observed  by  Sir  W.  Gull  a  considerable  dilatation  of  the  spinal 
canal  (Fig.  143)  was  found  in  the  cervical  region,  and  on  this  level  the 


FiQ.  143. 


Transverse  Section  of  the  Cervical  Enlargement  of  the  Spinal  Cord,  showing  a  central  cavity, 

WHICH  has  destroyed  consideuable  portions  of  the  anterior  GRAY  HORNS.     (After  Gull  ) 

gray  substance  of  the  cord  was  so  much  compressed  as  to  have  almost 
disappeared.  In  a  case  recorded  by  Westphal  the  cavity  was  said  to 
have  resulted  from  the  softening  of  a  gliosarcomatous  tumor,  but  in  a 
later  paper  by  the  same  author  it  is  admitted  that  the  tumor  was  most 
probably  a  mass  of  inflammatory  tissue. 


I 


MYOPATHIC    ATROPHIC    PARALYSES, 


4:59 


Treatment. — The  treatment  is  the  same  as  that  foi'  the  subacute 
ascending  general  paralysis  of  Duchenne. 

In  progressive  muscular  atrophy  the  spinal  cord  has,  according  to 
Eulenburg,  been  examined  in  forty-nine  cases,  and  out  of  these,  morbid 
changes  have  been  found  in  thirty-four,  while  the  cord  was  healthy  in 
fifteen  cases.  But  too  much  importance  must  not  be  attached  to  the 
cases  in  which  the  results  were  negative,  inasmuch  as  changes  may  have 
been  present  in  many  of  them,  and  been  overlooked  for  want  of  the 
requisite  skill  on  the  part  of  the  person  who  conducted  the  examination, 
while  it  is  certain  that  cases  have  been  included  in  these  statistics  which 
must  be  transferred  from  the  group  of  progressive  muscular  paralvsis 
to  the  juvenile  form  of  muscular  atrophy  described  by  Erb. 

Fig.  144. 


Transverse  Section  of  the  Cervical  Region  of  the  Spinal  Cord,  from  a  case  of  progressive 

muscular  atrophy.     (charcot.) 

A,  Left  anterior  gray  horn  ;  the   ganglion  cells  have  persisted,  but  are  much  altered  in  appearance. 

B,  Eight  anterior  graj'  horn,  almost  complete  atrophy  of  the  cells,  one  group  only  (6)  having  persisted. 


Attention  was  first  directed  by  Luys  to  the  morbid  changes  of  the 
gray  substance  of  the  spinal  cord  in  cases  of  progressive  muscular 
atrophy.  In  a  case  of  advanced  progressive  muscular  atrophy  he  found 
the  capillary  vessels  of  the  gray  substance  of  the  anterior  horns  increased 
in  number,  the  walls  of  the  vessels  thickened  and  surrounded  by  granu- 
lar exudation,  numerous  corpora  amylacea  scattered  through  the  gray 
substance,  and  disappearance  of  a  considerable  number  of  the  ganglion 
cells  and  disintegration  of  others.     The  degeneration  affected  the  left 


4(>0 


ATROPHIC    PARALYSES. 


anterior  cornu  principally,  this  localization  being  the  counterpart  of  the 
fact  that  the  atrophy  was  most  pronounced  on  the  left  side.  The  spinal 
cord  has  been  examined  in  six  cases  of  the  disease  by  Lockhart  Clarke, 
and  the  observations  of  Luys  have  been  confirmed  by  him  in  all  essential 
respects,  and  similar  observations  have  been  made  by  Dumenil,  Hayem, 
Charcot  and  Joffroy,  Pierret  and  Troisier,  and  others. 

In  a  case  reported  by  Charcot  the  ganglion  cells  of  the  left  anterior 
o-ray  horn  (Fig.  144,  A)  could  still  be  distinguished,  but  were  observed 
to  be  in  an  advanced  stage  of  atrophy.  In  the  right  anterior  horn 
(Fig.  144,  B),  however,  the  cells  could  only  be  distinguished  in  one 
group — the  postero-lateral  (Fig.  144,  b) — while  the  cells  of  the  remain- 
incp  oroup  were  completely  destroyed.  But  it  has  appeared  to  me  that 
too  little  attention  has  hitherto  been  paid  to  the  condition  of  the  central 
gray  column.  In  this  diagram  (Fig.  144)  the  left  central  column  is 
seen  to  be  intersected  by  enlarged  vessels,  and  that  of  itself  affords  some 
evidence  that  this  column  was  not  free  from  disease  in  the  section  from 
which  the  drawing  was  taken.     It  seems  to  me  likely  that  the  morbid 

Fig.   145. 


TnANSVERSE  Section  from  the  Middle  of  the  Cervical  Enlahgemest  of  the  Spinal  Coud,  from  an 

ADVANCED  CASE  OF  PROGRESSIVE  MUSCULAE  ATROPHY.       (YOUNO.) 

cc.  Central  canal ;  i,  Internal ;  al,  Antero-lateral,  nmXpl,  Postero-lateral  groups  of  ganglion  cells. 

process  begins  on  each  side  of  the  central  canal,  probably  in  tlie  tissues 
immediately  adjoining  the  central  artery,  and  that  it  extends  outwards 
and  forwards,  as  well  as  upwards  and  downwards  from  this  point  as  a 
centre.     In  a  transverse  section  of  the  middle  of  the  cervical  enlarge- 


MYOPATHIC    ATEOPHIC    PARALYSES, 


461 


uient  in  my  possession,  which  I  owe  to  the  kindness  of  Dr.  Dreschfeld, 
it  was  unmistakable  that  the  central  gray  column  Avas  more  diseased 
than  any  other  part  of  the  section.  This  column  was  traversed  bv  en- 
larged vessels,  and  almost  all  structure  was  obliterated,  while  the  various 
groups  of  ganglion  cells  on  the  anterior  horns  Avere  still  distinctly 
recognizable.  The  cells  of  the  median  area  and  the  marginal  cells  of 
the  other  groups  were  destroyed,  but  considerable  traces  of  the  laro-e 
cells  of  the  groups  were  still  distinctly  visible  (Fig.  145).  I  have  also 
observed  in  one  of  my  sections  a  streak  of  degeneration  to  pass  alono- 
the  posterior  branch  of  the  central  artery  and  into  the  substance  of  the 
posterior  horn,  and  this  may  explain  why  patches  of  cutaneous  Anal- 
gesia are  sometimes  met  with  in  progressive  muscular  atrophy.  In  the 
accompanying  woodcut  (Fig.  146)  borrowed  from  Leyden's  work  on 
the  diseases  of  the  spinal  cord,  it  is  also  distinctly  represented  that  the 
most  diseased  portions  occupy  the  central  column  of  the  cord,  and  that 
thence  the  disease  extends  laterally  to  the  anterior  gray  horns  and 
])etween  the  groups  of  ganglion  cells. 


Fig.  14ti. 


Transverse  Sectkix  of  the  Spinal  Cord  from  the  31iddle  of  the  Cervical  ExLARiiEMEXT,  siiowi.st; 

THAT  THE  CENTRAL  COLUMN  AND  A  LARGE  PORTION  OF  THE  ANTERIOR  GRAY  HORNS  ARE  DISEASED. 

(From  Leyden.  I 

The  anterior  roots  of  the  nerves  were  first  observed  to  be  diseased  by 
Cruveilhier  in  the  case  of  the  shoAvman  Le  Compte,  who  died  of  a  pro- 
gressive muscular  atrophy  of  five  year's  duration,  and  similar  observa- 
tions have  since  been  made  by  others.  The  peripheral  nerves  have 
likewise  been  found  diseased  by  Virchow,  Hayem,  Charcot  and  Joft'roy, 
Bamberger,  and  many  others.  The  changes  observed  consisted  of  hyper- 
plasia of  the  neurilemma,  multiplication  of  nuclei,  and  a  fibrillary 
thickening  of  the  sheath  of  Sclnvann. 


462  ATROPHIC    PARALYSES. 

In  addition  to  the  aflfection  of  the  anterior  horns  and  peripheral  fibres, 
the  posterior  columns,  the  posterior  horns,  the  posterior  roots,  and  the 
intervertebral  ganglia  have  been  found  in  a  state  of  degeneration.  The 
cervical  sympathetic  was  found  diseased  in  a  case  examined  by  Schnee- 
voo-t,  the  cervical  ganglia  were  almost  entirely  changed  into  fat  cells, 
while  the  cords  of  the  cervical  and  thoracic  sympathetic  abounded  in 
fat  cells  which  compressed  the  nerve  fibres.  More  or  less  similar  obser- 
vations were  made  by  Jaccoud,  Swarzenski  and  Dumenil. 

In  progressive  bulbar  paralysis  the  essential  morbid  changes  appear 
to  consist  of  a  degenerative  atrophy  of  the  ganglion  cells  of  the  gray 
nuclei  in  the  floor  of  the  fourth  ventricle.  The  cells  shrink  and  become 
filled  with  yellow  or  brown  pigment,  their  nuclei  disappear,  and  finally 
the  ceils  themselves  are  only  represented  by  angular,  glistening,  and 
pigmented  masses.  The  connective  tissue  is  found  to  be  increased  and 
to  contain  Gllige's  corpuscles ;  the  nuclei  and  Dieter's  cells  are  multi- 
plied, and  the  vascular  walls  are  hypertrophied  or  have  undergone 
fatty  degeneration. 

Fig.  147. 


NH w-'     -  -...  '"t?^^'  J  -  NH 


<«■ 


H 


R 


Portion  oi-  the  Gray  Substance  on  the  floor  op  the  fourth  ventricle  on  a  level  with  the  middle 
or  THE  Hypoglossal  Nucleus,  from  a  case  of  Progressive  Muscular  Atrophy  with  Bulbar  Paralysis, 

SHOWING  the  destruction  OF  THE  GANGLION  CeLLS  OF  THE  NUCLEI  OF  THE    HYPOGLOSSAL    AND    PnEU.MOOA.S- 

tric  Xerves  (NH).     (From  Leyden  ) 

R,  Jledian  raphe  ;  H,  H,  Filires  of  the  hypoglossal  nerves.     The  accessory  nuclei  have  evidently 

disappeared . 

The  nuclei  of  the  hypoglossal  nerves  appear  to  be  the  starting  point 
of  the  disease,  and  the  nuclei  of  the  spinal  accessory  and  pneumogas- 
tric   nerves  are  afterwards  invaded,  but  the  disease  does  not  always 
extend  to  the  nuclei  of  the  glosso-pharyngeal  nerves.     The  nuclei  of       _ 
the  fiicial  nerves  are  attacked  at  a  very  early  period  of  the  disease,  and       ■ 


MYOPATHIC    ATROPHIC    PARALYSES.  463 

the  nuclei  which  are  connected  with  the  inferior  branches  of  the  nerves, 
and  which  I  have  named  the  accessory  nuclei,  are  especially  liable  to 
be  invaded.  The  motor  nuclei  of  the  fifth  nerves  have  been  found 
affected,  but  the  nuclei  of  the  sixth  and  acoustic  nerves  and  the  tri- 
geminal sensory  nuclei  seem  never  to  suffer.  The  annexed  diagram 
(Fig.  147),  borrowed  from  Leyden,  represents  the  morbid  changes 
observed  in  the  medulla  oblongata  in  bulbar  paralysis.  Remnants  of 
the  fundamental  cells  of  the  hypoglossal  nuclei  may  still  be  observed, 
while  no  traces  of  the  accessory  nuclei  are  left.  This  would  seem  to 
indicate  that  the  morbid  process  begins  in  the  embryonic  tissue  which 
immediately  underlies  the  ependyma  of  the  fourth  ventricle,  and  that 
with  advance  of  the  disease  the  changes  extend  deeper  and  deeper  into 
the  gray  matter  and  among  the  oldest  formed  cells.  Other  changes 
have  been  described,  but  they  appear  to  be  secondary  to  the  alterations 
in  the  ganglion  cells.  Atrophy  of  the  roots  of  the  hypoglossal,  facial, 
and  spinal  accessory  nerves  was  discovered  by  the  earlier  observers 
with  the  naked  eye,  and  degenerative  atrophy  of  the  nerve  fibres  was 
subsequently  observed  on  microscopic  examination.  The  muscles  are 
found  to  undergo  essentially  the  same  degenerative  changes  which  are 
observed  in  progressive  muscular  atrophy.  The  anterior  pyramids  of 
the  medulla  oblongata  have  often  been  found  diseased,  and  the  morbid 
changes  were  generally  traced  upwards  into  the  pons  and  downwards 
into  the  antero-lateral  columns  of  the  spinal  cord.  It  is  probable  that 
in  all  these  cases  the  lower  extremities  were  affected  during  life  with  a 
spasmodic  paralysis.  The  bulbar  affection  is  often  associated  with 
lesions  of  the  anterior  gray  horns  of  the  spinal  cord,  indicating  a  com- 
plication during  life  with  progressive  muscular  atrophy. 

In  a  fatal  case  of  ophthalmoplegia  externa  reported  by  Mr.  J. 
Hutchinson,  degeneration  of  the  roots  of  the  oculo-motor  nerves  and 
disappearance  of  the  cells  from  their  nuclei  were  found,  at  the  post- 
mortem, by  Dr.  Gowers.  In  a  case  of  locomotor  ataxia  complicated  by 
ophthalmoplegia  externa,  reported  by  Dr.  Buzzard,  extensive  changes 
were  discovered  by  Dr.  Bevan  Lewis  in  the  nuclei  of  the  sixth  nerve 
and  in  the  ascendino;  root  of  the  fifth  nerve,  and  in  a  case  of  this 
kind  which  died  recently  under  my  care,  I  noted  the  disappearance  of 
cells  fi'om  the  nuclei  of  the  third  pair  of  nerves,  and  degenerative 
changes  in  the  ascending  and  descending  roots  of  the  fifth  nerve  and 
in  the  fasciculus  rotundus.  It  appears  likely  that  two  kinds  of  cases 
are  included  in  this  group.  In  the  one  the  ganglion  cells  of  the  nuclei 
of  the  ocular  nerves  undergo  a  primary  degeneration  just  as  occurs  in 
bulbar  nuclei  in  progressive  bulbar  paralysis,  while  in  the  other,  the 
primary  disease  is  found   in  the  cranial  homologues  of  the  posterior 


464 


ATEOPHIC    PARALYSES, 


root-zones,  the  ascending  and  descending  roots  of  the  fifth  nerve  and 
the  fasciculus  rotundus,  and  the  ganglion  cells  of  the  oculo-motor 
nerves  are  only  implicated  secondarily. 

In  pseudo-hypertrophic  paralysis  and  the  juvenile  form  of  progres- 
sive muscular  atrophy  the  spinal  cord  and  peripheral  nerves  are  normal 
or  show  only  minor  changes,  which  must  be  regarded  as  secondary  to 
the  changes  in  the  muscular  system. 

2.  Changes  in  the  Muscles. — When  a  peripheral  nerve  is  divided  or 
injured  the  muscle  supplied  by  it  undergoes  a  progressive  atrophy,  the 
various  degrees  of  which  have  already  been  described.  Essentially 
similar  changes  occur  in  the  muscles  in  the  various  forms  of  progressive 
multiple  neuritis,  but  in  reflex  paralysis  the  muscular  fibres  only  undergo 
a  simple  wasting  Avithout  proliferation  of  nuclei  or  destruction  of  the 


Muscular  Fibues  from  a  case  of  advanced  Infantile  Paralysis  withdrawn  bv  Leech's  trocar. 

(Young.) 
a,  Muscular  fibres  presenting  a  more  or  less  healthy  appearance  ;  h,  muscular  fibres,  soniewliat  atroi)liieil, 
and  with  granular  contents  ;  c,  muscular  fibres  greatly  atrophied,  but  presenting  faint  traces  of  transverse 

striation,  and  having  their  surfaces  thickly  studded  with  nuclei. 

fibres.  In  Landry's  paralysis,  also,  the  muscular  fibres  may  undergo 
some  degree  of  wasting,  but  they  have  not  been  found  much  altered  in 
their  structure.  In  the  acute  atrophic  spinal  paralysis  of  infants  and 
adults  the  muscles  undergo  essentially  the  same  changes  as  after  severe 
injury  of  a  peripheral  nerve.  When  a  portion  of  a  muscle  which  has 
undergone  advanced  atrophy  is  withdraAvn  by  means  of  Leech's  trocar, 
it  will  be  found,  as  shown  in  Fig.   148,  that  some  of  the  fibres  are 


J 


MYOPATHIC    ATROPHIC    PARALYSES.  465 

more  or  less  healthy  (a) ;  that  others  have  lost  their  normal  striation 
and  present  granular  contents,  but  are  not  much  diminished  in  size  (6) ; 
that  a  large  number  are  reduced  to  slender,  transparent  filaments,  while 
still  others  retain  a  faint  degree  of  their  transverse  striation,  but  have 
their  surfaces  thickly  studded  with  nuclei  (c).  The  nuclei  may  be  ob- 
served to  project  distinctly  from  the  surface  of  its  atrophied  fibre,  and  it 
is,  therefore,  probable  that  they  have  been  derived  from  either  the  nuclei 
of  the  sarcolemma  or  of  the  endoraysium.  In  chronic  atrophic  spinal 
paralysis  the  changes  in  the  muscles  are  never  so  well  marked  as  they 
are  in  the  acute  variety,  while  in  periependymal  myelitis  the  muscles 
have  not  been  carefully  examined. 

In  progressive  muscular  atrophy  the  muscles  have  been  found  vari- 
ously altered.  The  affected  muscles  are  generally  of  a  pale  red  or  rose 
color,  while  at  other  times  they  may  be  bufl"  or  ochre,  and  streaks  of 
adipose  tissue  may  be  seen  to  run  in  lines  between  the  fibres.  The 
muscles  are  wasted  in  various  degrees,  and  different  parts  of  the  same 
muscle  may  present  differences  in  the  degree  to  which  the  atrophy  is 
carried,  a  portion  being  sometimes  normal  while  the  rest  is  reduced  to 
a  fibrous  band. 

A  microscopical  examination  of  the  muscle  at  different  stages  of  the 
atrophy  shows  that  the  changes  begin  in  the  perimysium  internum  as  a 
hyperplastic  groAvth  of  the  interstitial  connective  tissue  in  its  finest 
ramification  among  the  single  primitive  fibres.  The  muscle  corpuscles 
are  increased  in  number,  and  swollen,  their  nuclei  are  multiplied,  and 
the  transverse  striation  becomes  faint,  while  the  fibres  present  a  granu- 
lar cloudiness.  Wasting  of  the  muscular  substance  goes  on  side  by 
side  Avitli  increase  of  the  interstitial  tissue,  a  process  which  ultimately 
leads  to  a  true  cirrhosis  of  the  muscle. 

In  pseudo-hypertrophic  paralysis  and  the  juvenile  form  of  progressive 
muscular  atrophy  the  hypertrophied  muscles  appear  as  yellow  fatty 
masses  of  tissue,  Avith  scarcely  a  trace  of  muscular  structure  left,  Avhile 
those  which  have  undergone  extreme  atrophy  may  appear  as  fibrous 
bands. 

The  first  muscular  change  which  takes  place  in  this  disease  consists 
of  an  increase  of  the  connective  tissue  which  separates  the  muscular 
bundles  from  one  another,  so  that  the  sheaths  of  the  muscular  bundles 
become  greatly  thickened.  There  is  also  a  corresponding  increase  of 
the  connective  tissue  which  passes  betAveen  the  fibres  themselves.  The 
comparatively  thick  masses  of  tissue  Avhich  noAv  separate  the  fibres  from 
one  another  consist  of  fibres  arranged  parallel  to  the  long  axes  of  the 
muscular  bundles,  mixed  Avith  a  considerable  number  of  embryonic 
cells  (Fig.  149,  e).     In  this  early  stage  the  muscular  fibres  themselves 

30 


466 


ATROPHIC    PARALYSES. 


do  not  undergo  any  manifest  changes,  except  that,  according  to  Du- 
chenne,  their  transverse  striation  becomes  fainter,  while  their  longi- 
tudinal striation  becomes  more  marked  (Fig.  149,  a).  The  second 
stage  of  the  change  consists  of  the  development  of  fat  cells  in  the 
connective  tissue  and  also  in  the  newly  formed  fibrous  tissue,  whereby 
the  muscular  fibres  become  widely  separated  from  one  another.  The 
muscular  fibres  now  become  atrophied  and  begin  to  disappear.  They 
become  narrower,   and,   indeed,   a  single  fibre  varies   in   diameter   at 


Muscular  Fibres  in  various  stages  of  degeneration,  from  a  case  of  Pseudo-hypertroi-hic  Paralysis. 

(Young.) 
a,  Muscular  fibres  only  slightly  changed,  showing  increase  of  the  muscle  corpuscles,  and  indistinctness 
of  the  transverse  striation  in  certain  parts  of  its  length  ;  h,  the  same  as  a,  Imt  more  atrophied  ;  c,  muscu- 
lar fibre  greatly  atrophied,  and  presenting  nuclei  at  intervals;  d,  atrophied  muscular  fibre,  with  its 
transverse  striation  unusually  distinct ;  e,  atrophied  fibre  surrounded  by  a  fibrillated  connective  tissue  rich 
in  nuclei ;  /and  g,  muscular  fibres  from  the  erector  spina-,  which  manifested  the  greatest  changes  to  the 
naked  eye.  These  fibres  appear  to  have  undergone  a  hyaline  change,  but  their  transverse  striation  is  still 
faintly  visible.     The  fibres  often  tapered  to  a  point,  sometimes  at  one  and  sometimes  at  both  ends. 

different  points  in  its  length.  The  transverse  striation  may  disappear 
in  the  narrower  fibres  and  be  replaced  by  granules  distributed  uniformly 
through  them.  The  fibrous  tissue  surrounding  the  fibres  contains  oat- 
shaped  nuclei  which  are  supposed  by  some  pathologists  to  be  derived 
from  the  empty  sheaths  of  muscular  fibres.  After  a  time  both  the 
muscular  fibres  and  the  newly  formed  fibrous  tissue  completely  disap- 
pear, and  the  entire  muscle  is  represented  by  fat  cells  like  those  of  an 


MYOPATHIC    ATROPHIC    PARALYSES.  467 

ordinary  lipomata,  but  may  subsequently  be  absorbed,  and  all  that  is 
left  of  the  muscle  is  connective  tissue  with,  perhaps,  a  few  traces  of 
muscular  fibres. 

The  fact  that  this  disease  is  accompanied  by  a  progressive  paralysis 
and  atrophy  of  muscles  has  led  authors  to  believe  that  the  essential 
morbid  changes  would  be  found  in  the  anterior  gray  horns  of  the  spinal 
cord,  and  slight  changes  have  been  discovered  in  some  of  the  cases 
Avhich  have  been  examined  post  mortem.  These  changes  have  not 
always  been  the  same  in  different  cases  and  are  likewise  so  slight  in 
degree  that  they  are  not  likely  to  be  essential  to  the  disease.  A  con- 
siderable number  of  cases  are  now  reported  in  which  the  spinal  cord 
and  peripheral  nerves  were  found  quite  healthy  after  being  examined 
by  the  most  competent  observers  and  with  the  aid  of  the  most  approved 
methods  of  research.  Under  these  circumstances  it  must  be  assumed 
that  the  muscular  atrophy  is  either  primary,  or  results  from  disease  of 
the  intramuscular  nerve  fibres  and  endings,  and  whatever  changes  are 
met  with  in  the  cord  are  either  secondary  to  the  muscular  disease,  or 
accidental.  And  if  the  cases  which  have  been  described  by  Erb  under 
the  name  of  "the  juvenile  form  of  progressive  muscular  atrophy"  be 
transferred  from  the  group  of  progressive  muscular  atrophy,  in  which 
many  of  them  have  hitherto  been  included,  to  that  of  pseudo-hyper- 
trophic  paralysis  then  we  have  on  the  one  hand  a  primary  disease  of  the 
ganglion  cells  of  the  spinal  cord,  and  on  the  other  a  primary  disease  of 
the  muscles  or  of  the  intramuscular  nerve  endings. 

The  tendons,  joints,  and  hones  are  liable  to  undergo  morbid  changes 
in  some  of  the  forms  of  atrophic  paralysis.  These  changes  are  probably 
best  marked  in  the  acute  atrophic  paralysis  of  infants.  In  this  affection 
the  tendons  appear  as  thin,  narrow  bands,  and  are  found  to  be  much 
atrophied  when  compared  with  corresponding  healthy  structures.  The 
hones  are  retarded  in  their  growth  when  the  disease  occurs  in  childhood  ; 
the  protuberances  and  processes  are  little  developed,  and  the  epiphyses 
are  shortened.  The  external  lamella  of  the  long  bones  is  thin  and  friable, 
while  the  medullary  portion  is  increased,  and  its  fiitty  contents  more 
abundant.  The  ligaments  are  thin  and  loose,  while  the  articular  ex- 
tremities of  the  bones  are  atrophied,  eroded,  and  their  cartilages  atten- 
uated. The  arteries  are  said  to  be  diminished  in  calibre.  The  skin 
and  the  circulatory  and  digestive  organs  are  normal  or  only  show  changes 
which  have  no  necessary  connection  with  the  spinal  disease.  Essentially 
similar  changes  occur  in  disease  of  the  peripheral  nerves. 

Morhid  Physiology. — The  ganglion  cells  of  the  anterior  gray  horns 
of  the  spinal  cord  are  the  trophic  centres  for  the  efferent  fibres  of  the 
peripheral  nerves  and  muscles,  and  they  also  appear  to  produce  an 


468  ATROPHIC    PARALYSES. 

influence  upon  the  nutrition  of  the  bones,  tendons,  and  joints.  A 
destructive  lesion  of  a  peripheral  nerve  severs  the  ganglion  cells  of  the 
anterior  horns  from  the  distal  portion  of  the  nerve  and  from  the  tissues 
to  which  the  efierent  fibres  are  distributed,  and  consequently  the  nutri- 
tion of  tissues  becomes  impaired.  In  reflex  paralysis  an  irritation  is 
conducted  through  afferent  fibres  to  the  motor  ganglion  cells  and  reflected 
by  them  outward  to  the  muscles ;  or,  as  suggested  by  Charcot,  the 
peripheral  irritation  may  exercise  an  inhibitory  influence  upon  the  func- 
tions of  the  ganglion  cells,  and  a  diminished  functional  activity  on  the 
part  of  these  cells  will  lead  to  a  lessened  nutrition  in  the  muscles. 
Ligature  of  the  hilus  of  the  kidney  in  animals  was  observed  by  Brown 
Sequard  to  cause  spasm  of  the  spinal  vessels,  and  from  the  results  of 
this  experiment  he  argued  that  urinary  paraplegia  is  caused  by  anj^niia 
of  the  spinal  cord.  Jaccoud  supposes  that  in  such  cases  the  paralysis 
is  caused  by  the  exhaustion  which  follows  over-excitement,  while  S. 
Weir  Mitchell  adopts  a  view  which  appears  to  be  a  combination  of  the 
theory  of  reflex  vascular  spasm,  and  that  of  exhaustion.  It  has  been 
found  by  Lewisson  that  when  the  uterus,  one  kidney,  or  a  fold  of  the 
intestine  of  the  hare  is  strongly  compressed,  after  exposure,  a  paralysis 
of  the  inferior  extremities  results,  which  persists  so  long  as  the  pressure 
is  maintained  and  disappears  immediately  on  its  being  removed.  This 
experiment  shows  that  the  paralysis  is  caused  by  a  functional  lesion  of 
the  cord,  consisting  most  probably  of  an  inhibitory  influence  exerted 
upon  the  motor  ganglion  cells.  When  myelitis  occurs  it  is  an  ascending 
myelitis. 

Acute  atrophic  spinal  paralysis  is  one  of  those  diseases  the  morbid 
anatomy  of  which  lias  largely  contributed  to  clear  up  our  knowledge  of 
the  functions  of  the  anterior  gray  horns.  The  multipolar  cells  probably 
constitute  ganglionic  centres  both  for  reflex  action  and  for  the  trans- 
mission  of  impulses  received  from  the  cortex  through  the  pyramidal 
tracts,  and  when  they  are  destroyed  both  reflex  actions  and  voluntary 
actions  are  impaired  or  abolished  according  as  the  destruction  of  the 
cells  is  incomplete  or  complete.  Destruction  of  the  ganglion  cells  is 
also  followed  by  various  trophic  changes  in  the  muscles,  bones,  tendons, 
and  joints.  The  ganglion  cells  which  constitute  the  spinal  centre  for 
the  regulation  of  the  movements  of  a  muscle  appear  also  to  form  its 
trophic  centre.  But  most  muscles  are  connected  with  fundamental  and 
accessory  cells  and  it  is  only  when  the  connection,  between  the  former 
and  the  muscle,  is  severed  that  its  motor  power  and  nutrition  suffer  pro- 
foundly. The  acute  nature  of  the  lesion  in  acute  atrophic  paralysis  is 
well  calculated  to  sever  the  muscles  from  their  connections  with  the 
fundamental  cells,  even  if  the  latter  were  to  remain  themselves  entirely 


MYOPATHIC    ATROPHIC    PARALYSES.  469 

unaffected,  and  consequently  the  clinical  features  of  the  paralysis  are 
very  similar  to  the  paralysis  which  results  from  severe  lesions  of  the 
peripheral  nerves. 

The  case  is  wholly  different  when  we  have  to  do  Avith  a  chronic  and 
progressive  affection  like  progressive  muscular  atrophy,  in  which  the 
accessory  cells  are  first  attacked,  and  the  disease  invades  by  slow  and 
successive  steps  the  fundamental  cells.  In  such  a  disease  the  symptoms 
of  paralysis  and  atrophy  may  be  expected  to  pursue  a  totally  different 
course  from  that  which  obtains  in  acute  atrophic  spinal  paralysis. 

In  progressive  muscular  atrophy  fibre  after  fibre  of  the  muscles 
attacked  become  diseased  in  correspondence  with  a  similar  progi-essive 
invasion  of  the  ganglion  cells  and  their  processes,  and  the  consequence 
is  that  so  long  as  the  healthy  fibres  predominate  over  the  diseased 
fibres  so  long  Avill  the  muscle  give  normal  reactions  to  electrical  examina- 
tion. But  in  acute  atrophic  spinal  paralysis  all  the  fibres  of  a  muscle 
are  more  or  less  simultaneously  attacked  and  consequently  the  muscle 
gives  the  reaction  of  degeneration  at  a  very  early  period  of  the  disease. 

Treatment. — In  the  treatment  of  the  various  forms  of  atrophic  paral- 
ysis the  first  indication  is  to  remove  the  exciting  cause.  In  carrying 
out  this  indication  in  cases  of  paralysis  of  peripheral  nerves  consider- 
able scope  is  afforded  for  various  kinds  of  surgical  interference,  such  as 
bringing  together  by  means  of  suture  the  ends  of  divided  nerves,  the 
removal  of  tumors  and  diseased  bones  which  compress  or  otherwise 
injure  nerve  trunks.  When  the  paralysis  is  of  rheumatic  origin  anti- 
phlogistic treatment  must  be  adopted  in  the  early  stages  of  the  disease, 
and  when  it  is  caused  by  the  presence  of  lead,  alcohol,  or  other  poison, 
means  must  be  taken  for  withdrawing  the  patient  from  the  influence  of 
the  deleterious  agent,  and  for  eliminating  it  from  the  system.  If  the 
paralysis  is  of  syphilitic  origin,  mercury  and  iodide  of  potassium  must 
be  prescribed  either  separately  or  combined.  In  the  early  stage  of  every 
form  of  acute  spinal  atrophic  paralysis  a  mild  antiphlogistic  treatment 
must  be  adopted. 

If  the  nature  of  the  disease  be  detected  at  an  early  period,  an  ice 
bag  may  be  applied  to  the  spine.  In  the  early  stage  of  the  atrophic 
paralysis  of  infancy  ergotine  has  been  employed  subcutaneously  in  doses 
of  one-fourth  of  a  grain  for  a  child  from  one  to  two  years  of  age,  one- 
third  of  a  grain  for  one  from  three  to  five  years,  half  a  grain  for  children 
from  five  to  ten  years  of  age,  and  a  grain  for  patients  upwards  of  ten 
years  of  age,  the  dose  being  repeated  either  daily  or  twice  a  day. 
Belladonna  has  also  been  employed  with  apparent  benefit  in  this  stage 
of  the  affection.  After  the  fever  has  subsided  iodide  of  potassium  may 
be  administered   in  appropriate  doses  with  the  view  of  promoting  the 


470  ATEOPHIC    PARALYSES. 

absorption  of  effused  products,  while  mild  counter-irritants  might  be 
applied  along  the  spine. 

In  the  latter  stages  of  acute  cases  and  in  all  chronic  cases  of  atrophic 
paralysis  stimulating  treatment  must  be  adopted.  A  nutritious  and 
abundant  diet  should  be  prescribed  along  with  prolonged  sojourn  in  the 
open  air,  mountainous  or  sea-air  being  especially  useful.  The  thermal 
springs  of  Wildbad,  Teplitz,  and  Gastein,  have  been  specially  recom- 
mended, and  sulphur  baths  have  also  been  found  useful. 

Electrical  treatment  is  more  useful  in  the  treatment  of  the  various 
forms  of  atrophic  paralysis  than  in  that  of  any  other  variety  of  paralysis. 
In  the  spinal  atrophic  paralysis  the  constant  current  should  be  made  to 
pass  through  the  diseased  area  of  the  cord  immediately  after  the  fever 
has  subsided.  If  the  leg  alone  be  affected,  the  current  should  be  applied 
over  the  lumbar  enlargement;  if  an  arm  only  be  affected,  the  cervical 
enlargement  should  ))e  acted  upon,  and  if  the  muscles  of  the  trunk 
suffer  likewise,  the  whole  dorsal  region  of  the  cord  should  be  included 
in  the  circuit.  In  order  to  reach  the  cord  it  is  better  to  place  one  pole 
on  the  spine,  and  to  apjily  the  other  to  the  anterior  surface  of  the  trunk. 
The  electrodes  should  be  large,  the  one  placed  over  the  back  being  large 
enough  to  cover  the  entire  diseased  area.  The  force  of  the  current 
should  be  gentle,  and  the  application  continued  for  from  three  to  ten 
minutes  according  to  the  extent  of  the  lesion.  The  local  application  of 
electricity  to  the  diseased  nerves  and  muscles  is  useful  in  all  cases  in 
which  degenerative  changes  have  occurred  in  the  muscles.  So  long  as 
the  muscles  and  nerves  have  not  entirely  lost  their  faradic  contractility 
the  local  application  of  the  faradic  current  will  be  of  service.  But  as 
a  rule  the  constant  is  superior  to  the  interrupted  current,  being  in 
most  cases  the  only  agent  which  will  evoke  nuiscular  response.  Appro- 
priate gymnastic  exercises  of  the  affected  muscles  when  they  are  not 
completely  paralyzed,  and  shampooing  and  friction,  with  or  without 
stimulating  liniments,  may  be  employed  as  adjuncts  to  the  electrical 
treatment.  After  the  chronic  stage  of  atrophic  paralysis  is  fully  estab- 
lished internal  remedies  do  not  appear  to  do  much  good.  The  most 
usual  remedies  for  chronic  cases  are  phosphorus  Avith  cod-liver  oil, 
arsenic,  and  tonics  like  iron  and  quinine,  but  these  agents  probably  do 
good  only  in  so  far  as  they  help  to  improve  the  general  health.  The 
use  of  strychnine  has  been  advocated  in  cases  of  infantile  atrophic 
paralysis,  especially  in  the  form  of  subcutaneous  injection,  but  I  have 
never  seen  any  good  results  attend  its  employment.  When  serious 
deformities  result  from  paralysis  of  certain  groups  of  muscles  the  case 
should  be  placed  under  the  care  of  the  orthopaedic  surgeon. 


CHAPTEE    YIII. 

THE  SPASMODIC  PARALYSP:S. 
I.  PAPxAPLEGI^. 

1.  Primary  Lateral  Sclerosis  (Tabes  Dorsalis  Spasmodica 
(Charcot),  Spasmodic  Spinal  Paralysis). 

Etiology. — A  hereditary  tendency  to  the  disease  can  occasionally  be 
traced.  Dr.  Morgan  records  the  case  of  a  man  suffering  from  the 
typical  symptoms  of  lateral  sclerosis,  whose  brother  was  similarly 
affected,  while  a  sister  of  his  was  said  to  have  died  of  the  same  disease. 
Primary  lateral  sclerosis  appears  to  occur  rather  more  frequently  in 
males  than  in  females.  By  far  the  larger  number  of  cases  begin  between 
the  ages  of  thirty  and  fifty  years.  A  spasmodic  paralysis  of  the  lower 
extremities  of  congenital  origin  is  frequently  met  with  in  children, 
but  the  symptoms  in  these  cases  are  caused  most  probably  by  a  cere- 
bral lesion. 

The  exciting  causes  are  unknown,  although  it  is  very  probable  that 
exposure  to  cold,  injuries  of  the  spine,  lead  poisoning,  and  syphilis 
may  cooperate  as  factors  in  the  production  of  the  disease.  It  seems  to 
be  caused  sometimes  by  the  use  of  a  species  of  vetch — the  lathyrus 
cicera — as  a  chief  article  of  diet. 

Symptoms. — The  first  symptom  is  a  paresis  of  the  inferior  extremi- 
ties, which  may  be  equal  in  both  or  more  pronounced  in  one  than  in 
the  other,  and  the  only  effect  of  which  is  to  render  walking  somewhat 
difficult,  especially  on  getting  out  of  bed  in  the  morning.  The  patient 
complains  that  he  is  soon  fatigued,  and  that  his  limbs  are  heavy,  while 
his  o'ait  becomes  drao-gino;  and  difficult.  On  lying  down  at  night, 
especially  after  being  fatigued,  the  legs  begin  to  shake,  and  as  the  dis- 
ease advances  the  tremors  may  be  so  extensive  and  violent  as  to  throw 
the  whole  body  into  a  convulsive  trembling,  which  has  been  named 
spinal  epilepsy.  These  tremors  may  be  readily  excited  by  pushing 
against  the  toes  so  as  to  produce  dorsal  flexion  of  the  foot.  Muscular 
tension  is  developed  at  an  early  period  of  the  disease;  at  first  the  ten- 
sion, which  is  only  present  when  provoked  by  passive  movement  of  the 
lower  extremities,  may  be  overcome  by  increasing  the  pressure,  and  it 


472  THE    SPASMODIC    PARALYSES. 

can  be  considerably  diminished  by  repeated  movements,  but  after  a 
time  the  muscles  become  tense  during  voluntary  efforts ;  the  paresis 
then  seems  to  be  greater  than  it  is  in  reality,  and  the  movements  of 
the  affected  limbs  become  stiff  and  difficult. 

As  the  disease  advances  the  muscular  tension  increases  to  permanent 
rigidity,  and  a  high  degree  of  contracture  results.  The  lower  extremi- 
ties are  maintained  in  a  position  of  rigid  extension,  the  thighs  are  also 
held  rigidly  together  by  contracture  of  the  adductors,  the  feet  are  in  a 
position  of  extreme  talipes  equino-varus,  but  the  toes  are  generally 
strongly  flexed.  The  rigid  immobility  of  the  foot  is  now  and  then 
interrupted  by  attacks  of  trembling,  which  are  excited  by  every  move- 
ment of  the  extremity. 

The  Spasmodic  Gfait  or  Spastic  Walk. — The  gait  of  the  patient  is 
rendered  quite  characteristic  by  the  combined  paresis,  stiffness,  and 
tremors  of  the  lower  extremities.  The  foot  seems  to  cling  to  the 
ground,  from  which  it  is  detached  Avith  difficulty,  and  it  is  made  to  slide 
forwards,  and  the  toes  produce  a  characteristic  scraping  noise.  The 
presence  of  lateral  sclerosis  may,  indeed,  be  sometimes  recognized 
without  seeing  the  patient  by  listening  to  the  scraping  or  shuffling 
noise  which  accompanies  each  step,  the  "shuffle"  in  hemiplegia  being 
only  heard  during  alternate  steps.  Owing  to  the  rigidity  of  the  lower 
extremities  in  extension  the  necessary  elevation  of  the  passive  leg  is 
usually  obtained  by  an  upward  rotation  of  the  pelvis,  W'hich  causes  the 
body  to  be  strongly  inclined  to  the  side  of  the  active  leg,  and  the 
alternate  inclination  of  the  body  from  one  si<le  to  the  other  during  suc- 
cessive steps  gives  rise  to  a  '•  waddling  gait."  In  other  cases  the 
necessary  elevation  of  the  passive  foot  is  obtained  partly  or  wholly  by 
an  unusual  degree  of  elevation  of  the  heel  of  the  active  leg,  and  in  these 
cases  the  gait  has  a  peculiar  hopping  character.  When  the  body  is  in- 
clined from  one  side  to  the  other  in  locomotion,  the  passive  foot  advances 
not  directly  forwards,  but  forwards  and  outwards  in  a  semicircular  man- 
ner, and  on  being  brought  to  the  ground  it  is  dragged  over  to  the 
opposite  side  in  front  of  the  other  leg  by  the  predominant  action  of 
the  adductors  over  their  antagonists,  while  the  foot  is  also  often  in- 
verted by  overaction  of  the  inward  rotators  of  the  thigh.  In  long- 
standing cases  the  patient  experiences  great  difficulty  in  disentangling 
the  toes  of  the  foot  about  to  be  advanced  from  the  heel  of  the  one 
which  has  just  been  brought  to  the  ground,  and  in  the  effort  to  accom- 
plish this  the  calves  of  both  legs  become  strongly  contracted,  the  patient 
is  elevated  on  tiptoes,  and  a  degree  of  ankle-clonus  may  be  induced 
which  suffices  to  give  rise  to  alternate  elevations  and  depressions  of  the 
body,  and  when  at  last  the  toes  of  the  posterior  are  disengaged  from  the 


PARAPLEGIA.  473 

heel  of  the  anterior  foot,  and  the  passive  leg  is  being  moved  forwards 
in  the  semicircular  manner  already  described,  the  foot  is  seized  with  a 
trembling  which  may  extend  to  the  trunk  and  be  so  violent  as  to  agitate 
the  whole  body.  In  aggravated  cases  of  this  kind  the  patient  is  quite 
unable  to  maintain  the  erect  posture  unsupported.  On  standing  the 
patient  rests  on  the  tips  of  his  feet,  the  body  is  inclined  forwards,  and 
the  arms  are  propped  up  by  crutches,  or  are  supported  by  two  sticks 
which  are  held  well  in  front  of  the  patient,  and  Avith  an  outward  inclina- 
tion. As  the  disease  gradually  extends  upwards  the  abdominal  muscles 
become  prominent  and  tense,  and  at  the  same  time  a  kind  of  lordosis 
is  produced  by  spasm  of  the  lumbar  muscles. 

When  the  upper  extremities  are  affected  the  paretic  condition  of  the 
hands  manifests  itself  by  the  inaptitude  of  the  patient  to  seize  small 
objects.  The  digits  are  at  times  forcibly  flexed  into  the  palm,  while  a 
successive  invasion  of  the  muscles  of  the  hands,  forearms,  and  arms 
causes  the  upper  extremity  to  become  rigid  and  immovable  in  positions 
of  extension  and  pronation,  and  to  be  strongly  drawn  to  each  side  of 
the  body. 

Although  the  disease  usually  begins  in  the  lower  extremities  and 
pursues  an  ascending  course,  yet  occasionally  the  symptoms  are  de- 
veloped in  a  different  order.  In  some  cases  the  paresis  passes  from  a 
lower  extremity  to  the  upper  one  of  the  same  side,  and  this  hemiplegic 
condition  may  persist  for  many  years  before  the  other  loAver  extremity 
is  attacked.  In  a  few  cases  the  disease  begins  in  the  upper  extremities 
and  pursues  a  descending  course. 

The  tendon  and  periosteal  reactions  are  much  exaggerated  in  this 
disease.  The  patellar  tendon-reaction  and  ankle-clonus  are  elicited  with 
undue  readiness  in  the  usual  way,  and  the  tremors  induced  may  become 
diffused  over  the  whole  body.  The  quadriceps  femoris  and  the  adductors 
of  the  thigh  may  be  excited  to  contract  by  tapping  the  broad  end  of  the 
tibia,  and  the  contractions  may  extend  to  the  adductors  of  the  opposite 
thigh.  The  adductors  of  the  thigh  may  often  be  made  to  contract  by  tap- 
ping over  the  region  of  the  lumbar  vertebrtB,  and  the  tibialis  posticus, 
semitendinosus,  and  other  muscles  by  striking  their  tendons.  The  ten- 
don reactions  are  in  like  manner  increased  in  the  upper  extremities  when 
once  they  are  implicated.  They  can  be  elicited  in  the  biceps  and 
triceps  by  striking  their  tendons,  and  the  former  may  be  made  to  con- 
tract by  tapping  the  lower  end  of  the  radius,  and  the  latter  by  tapping 
the  lower  end  of  the  ulna.  The  posterior  portion  of  the  deltoid  often 
contracts  along  with  the  triceps  when  the  lower  end  of  the  ulna  is 
lightly  struck.  The  flexors  of  the  wrist,  the  extensors  of  the  wrist, 
and   the  supinator  longus   can  each  be  made  to  contract  by  ta))ping 


474  THE    SPASMODIC    PARALYSES. 

their  tendons  at  the  wrist,  while  the  interossei  may  sometimes  be  made 
to  contract  by  striking  the  ends  of  the  metacarpal  bones. 

The  cutaneous  reflexes  appear  to  be  occasionally  increased,  but  they 
are  generally  normal  or  diminished.  The  electrical  excitability  of  the 
motor  nerves  may  manifest  slight  quantitative  but  never  qualitative 
changes;  the  excitability  of  the  muscles  is  slightly  diminished  to  both 
currents. 

Sensory  disorders  are  absent  throughout  the  whole  course  of  the 
disease ;  the  functions  of  the  bladdei-,  rectum,  and  sexual  organs  are 
unaffected  ;  and  there  are  no  vaso-motor  disturbances  or  nutritive  aflfec- 
tions  of  the  muscles  or  skin,  and  no  bedsores. 

The  course  of  the  disease  is  ahnost  always  very  chronic,  and  months 
or  years  may  elapse  before  it  can  even  be  recognized  with  certainty. 
The  disease  occasionally  ends  in  recovery,  but  in  uncomplicated  cases 
the  symptoms  slowly  and  gradually  progress  until  after  many  years  the 
patient  is  rendered  quite  helpless,  but  even  then  death  generally  occurs 
from  accidental  causes  or  intercurrent  diseases. 


2.  Amyotrophic  Lateral  Sclerosis. 

Etiology. — Very  little  is  known  Avith  regard  to  the  causation  of  this 
disease,  but  persons  of  middle  age  are  most  frequently  attacked.  Seelig- 
miiller,  however,  met  with  the  typical  form  of  the  disease  in  four  children 
of  the  same  family,  and  in  all  of  them  the  symptoms  appeared  for  the 
first  time  in  early  childhood. 

Symptoms. — In  this  disease  the  symptoms  of  primary  lateral  sclerosis 
are  complicated  by  a  progressive  muscular  atrophy.  The  symptoms 
are,  indeed,  more  allied  to  those  of  the  latter  than  to  those  of  the  former 
disease,  but  as  it  would  not  be  possible  to  understand  the  significance  of 
the  spastic  phenomena  until  the  clinical  features  of  primary  lateral 
sclerosis  had  been  described,  it  has  been  found  convenient  to  consider 
amyotrophic  lateral  sclerosis  in  this  place. 

The  disease  often  begins  with  premonitory  symptoms  of  formication 
and  numbness  in  the  upper  extremities,  but  it  is  soon  observed  that  these 
extremities  are  feeble,  and  that  their  muscles  are  undergoing  a  rapid 
and  uniformly  distributed  atrophy,  which  is  accompanied  by  fibrillary 
twitchings.  Muscular  tension  and  contractures  are  soon  superadded  to 
the  paresis  and  atrophy,  and  the  affected  extremities  are  brought  into 
permanently  deformed  positions.  The  arm  is  applied  to  the  trunk ;  the 
forearm  is  semiflexed  and  pronated ;  the  hand  is  flexed  on  the  foreann  ; 
and  the  different  segments  of  the  fingers  are  flexed  upon   one  another 


I 


\ 


PARAPLEGIA.  475 

and  upon  the  metacarpal  bones  (Fig.  150) ;  while  any  attempt  to  give 
passive  movements  to  the  limb  at  any  of  the  articulations  provokes 
muscular  tension  and  resistance.  When  the  patient  elevates  the  arm 
by  a  voluntary  effort,  the  extremity  becomes  agitated  by  tremors,  not 
unlike  those  which  occur  in  sclerosis  in  patches.  In  advanced  cases  the 
thenar  and  hypothenar  eminences  become  flattened ;  the  palm  of  the 
hand  becomes  excavated ;  the  forearm  and  arm  may  be  reduced  almost 
to  a  skeleton,   but  the  spasmodic    rigidity  becomes  less   pronounced, 

Fig.  150. 


Attitude  of  the  Hand  and  Forearm  in  AMVOTROPiirc  Lateral  Sclerosis.     (After  Charcot.) 

although  even  now  the  limbs  may  maintain  the  forced  attitudes  in  which 
they  have  been  held  so  long. 

In  some  patients  the  head  is  fixed  by  spasmodic  rigidity  of  the  muscles 
of  the  neck  so  that  it  cannot  be  moved  in  any  direction.  The  contrac- 
ture may  also  extend  to  the  temporal  muscles,  and  then  the  mouth  can 
only  be  opened  to  a  limited  degree. 

After  a  period  of  from  two  to  six  or  nine  months  the  lower  extremities 
become  affected  by  paresis,  which  may  be  preceded  or  accompanied  for 
a  longer  or  shorter  period  by  formication  and  numbness  of  the  limbs. 
The  paresis  of  the  lower  extremities  is  not  at  first  accompanied  by 
muscular  atrophy,  but  the  symptoms  are  those  of  a  pure  lateral  sclerosis, 
and  consist  of  muscular  tension,  contractures  with  the  limbs  held  rigid 
in  the  position  of  extension,  tremors  on  voluntary  or  reflex  movements 
of  them,  ankle-clonus,  and  exaggerated  tendon-reactions.  The  rigidity 
of  the  muscles  of  the  lower  extremities  soon  become  so  great  that  walk- 
ing is  impossible,  and  the  patient  becomes  helpless  and  bedridden.  After 
a  time  even  the  muscles  of  the  lower  extremities  undergo  a  diffused 
atrophy  with  fibrillary  twitchings,  the  contractures  diminish,  and  the 
limbs  become  flaccid  and  powerless,  and  lie  immovable  in  any  position 
in  which  they  may  be  placed.     The  third  stage  of  the  disease  is  char- 


4:76  THE    SPASMODIC    PAEALYSES. 

acterized  by  the  appearance  of  bulbar  paralysis  which  pursues  the  usual 
progressive  and  fatal  course,  and  the  patient  ultimately  dies  from  the 
circulatory  and  respiratory  disorders  caused  by  implication  of  the  nuclei 
of  the  pneumogastric  nerves. 

But  altliough  the  symptoms  usually  begin  in  the  upper  extremities  a 
few  cases  are  reported  in  which  the  phenomena  of  bulbar  paralysis  took 
the  precedence,  and  the  muscles  of  the  upper  extremities  became  para- 
lyzed and  atrophied  at  a  subsequent  period,  while  those  of  the  lower 
extremities  remained  the  subjects  of  a  spasmodic  paralysis  only  until 
the  terminal  period  of  the  disease. 

Amyotrophic  lateral  sclerosis  develops  rapidly,  and  generally  causes 
death  in  from  one  to  three  years,  differing  in  this  respect  from  progres- 
sive muscular  atrophy,  which  may  extend  over  a  period  of  from  eight  to 
twenty  years. 

3.  Secondary  Lateral  Sclerosis. 

Lateral  sclerosis  occurs  as  a  secondary  disease  in  transverse  myelitis 
and  in  various  diseases  of  the  medulla  oblongata,  pons,  and  brain. 
The  symptoms  of  secondary  degeneration  of  the  pyramidal  tract  of  the 
spinal  cord  will  be  described  in  detail  when  the  primary  lesions  from 
which  it  results  are  under  discussion.  It  will  suffice  at  present  to  say 
that  if,  to  the  motor  symptoms  of  lateral  sclerosis  already  described,  any 
sensory  disorders,  muscular  atrophy,  or  disturbances  of  the  functions  of 
the  bladder  and  rectum  be  superadded,  then  the  case  is  not  an  exam])le 
of  the  primary  disease, 

II.  HEMIPLEGI.E. 

1.  Ordixary  Hemiplegia. 

Hemij)legia  consists  of  paralysis  of  one  half  of  the  body,  although 
many  of  the  muscles  are  either  not  implicated  or  only  temporarily 
weakened.  The  paralysis  is,  as  a  rule,  limited  to  the  arm,  leg,  part  of 
the  face,  and  half  of  the  tongue.  The  muscles  chiefly  aff'ected  in  facial 
paralysis  of  cerebral  origin  are  the  buccinator,  orbicularis  oris,  and  the 
straight  muscles  which  pass  to  the  angle  of  the  mouth  and  nose  on  the 
paralyzed  side ;  while  the  occipito-frontalis,  corrugator  supercilii,  and 
orbicularis  oculi  remain  almost  entirely  unaff'ected.  Paralysis  of  the 
hypoglossal  nerve  is  manifested  by  a  difficulty  in  executing  certain 
movements  of  the  tongue,  and  by  a  deviation  of  the  point  to  the  sound 
side  on  protrusion,  because  the  base  is  dragged  further  forwards  on  the 
healthy  than  on  the  paralyzed  side.     It  is  often  stated  that  the  muscles 


HEMIPLEGI^E.  477 

of  the  trunk  are  unaffected  in  hemiplegia,  but  in  severe  cases  the  inspira- 
tory muscles  act  much  less  freely  on  the  paralyzed  than  on  the  healthy 
side  for  the  first  few  days  of  the  attack. 

2.  Hemiplegia  and  Hemian.t.sthesia. 

It  has  for  some  time  been  observed  as  a  clinical  fact  that  those  cases 
of  hemiplegia  in  Avhich  the  leg  is  more  paralyzed  than  the  arm  are 
^associated  Avith  hemianivsthesia.  In  such  cases,  however,  the  special 
senses  are  not  very  seriously  implicated. 

3.  Hemiplegia,  Hemianesthesia,  and  Hemianopsia. 

Some  cases  of  hemiplegia  in  which  the  arm  is  more  paralyzed  than 
the  leg  are  accompanied  by  hemiannesthesia.  In  these  cases  the  para- 
lyzed limbs  are  often  affected  by  choreoid  movements  and  the  cutaneous 
sensory  disorders  are  accompanied  by  disturbances  of  the  special  senses. 
The  sense  of  sight  is  variously  affected ;  in  some  there  is  a  restriction 
of  the  fields  of  vision  on  both  sides,  but  it  is  most  marked  on  the  side  of 
the  paralyzed  limbs,  while  in  others  a  well-defined  bilateral  homonymous 
hemianopsia  is  present,  the  blind  portions  of  the  fields  of  vision  being 
on  the  side  of  the  paralyzed  limbs.  In  certain  cases  of  hemiplegia  and 
hemiaUcTesthesia  which  come  on  with  severe  apoplectic  symptoms,  one 
eyeball  may  be  directed  downwards  and  outwards,  and  the  other  upwards 
and  somewhat  outwards.  Such  cases  may  live  for  many  days  or  weeks 
without  the  patient  regaining  a  sufficient  degree  of  consciousness  to 
render  it  possible  to  determine  whether  hemianopsia  is  or  is  not  present. 
Another  curious  symptom  which  is  sometimes  present  is  that  the  pupils 
may  be  found  to  dilate  to  light  and  to  contract  when  shaded ;  but  as  the 
eyeballs  are  almost  constantly  moving,  it  is  probable  that  the  changes  in 
the  diameter  of  the  pupils  are  to  be  regarded  as  an  associated  move- 
ment and  not  as  a  reflex  action.  In  these  cases  repeated  paroxysms  of 
Cheyne-Stokes  breathing  may  occur,  and  all  of  them  that  have  come 
under  my  observation  have  proved  fatal. 

4.  Crossed  Hemiplegia. 

In  cro.ssed  hemiplegia  the  muscles  supplied  by  one  or  other  of  the 
cranial  motor  nerves  are  paralyzed  on  one  side  and  the  limbs  on  the 
opposite  side  of  the  body.  The  cranial  nerves  most  frequently  affected 
in  this  form  of  paralysis  are  the  seventh  and  the  third  nerves ;  when 
the  first  of  these  is  affected  the  face  is  paralyzed  on  one  side  and  the 


478  THE    SPASMODIC    PARALYSES. 

limbs  on  the  other,  and  when  the  last  of  these  is  attacked  the  muscles 
supplied  by  the  oculo-motor  nerve  are  paralyzed  on  one  side  and  the  limbs 
on  the  other  side  of  the  body. 

5.  Hemiplegia  and  Post-hemiplegic  Spasms. 

In  hemiplegia  the  paralysis  is  accompanied  by  spasm  of  the  affected 
muscles.  These  may  be  either  a,  tonic,  6,  combined  tonic  and  clonic, 
or  c,  clonic  spasms.  In  addition  Ave  must  specially  consider  d,  spasm 
as  it  occurs  in  the  various  forms  of  the  spasmodic  paralysis  of  infancy. 

a.   Tonic  Spasms. 

These  spasms  may  be  divided  into  (1)  carhj,  and  (2)  late  ru/iditi/. 

(1)  Early  rigidity  consists  of  a  tonic  spasm  of  the  paralyzed  muscles, 
which  may  either  occur  at  the  time  of  the  hemorrhage  or  a  few  days 
subsequently  during  the  inflammatory  reaction.  Early  rigidity  is  some- 
times so  slight  as  only  to  be  manifest  when  passive  movement  of  the 
paralyzed  extremity  is  made,  while  at  other  times  it  maintains  both 
extremities  in  fixed  positions  of  flexion,  and  any  attempt  to  extend  the 
limbs  only  increases  the  spasm.  This  form  of  rigidity  generally  dis- 
appears soon,  but  it  occasionally  persists  for  weeks  or  months. 

(2)  Late  rigidity  corresponds  in  its  essential  features  to  the  spasmodic 
rigidity  of  primary  lateral  spinal  sclerosis,  and,  like  it,  is  attended  with 
exaggeration  of  the  tendon-reactions  and  periosteal  reflexes.  When  the 
lower  extremities  are  affected  the  patellar  tendon-reaction  is  in  excess, 
ankle-clonus  is  readily  elicited,  and  corresponding  phenomena  may  be 
obtained  in  the  upper  extremity  when  it  is  the  subject  of  contracture. 
When  the  loss  of  voluntary  power  is  complete  the  rigidity  is  more  or 
less  constant,  although  it  is  in  most  cases  diminished  during  sleep  and 
increased  during  voluntary  efforts  and  emotional  disturbances.  The 
attitudes  assumed  by  the  limbs  affected  with  late  rigidity  differ  consider- 
ably in  different  cases,  but  on  the  whole  they  conform  to  the  rule  observed 
in  almost  all  spasmodic  affections ;  namely,  that  flexion  predominates 
in  the  upper,  and  extension  in  the  lower  extremity. 

The  Hemiplegie  Cfait. — When  the  muscles  of  the  paralyzed  lower 
extremity  have  acquired  a  certain  degree  of  rigidity,  the  patient  is  able 
to  walk  by  the  aid  of  a  stick,  even  if  the  voluntary  paralysis  of  the 
affected  side  remain  complete.  The  patient  on  standing  leans  towards 
the  healthy  side,  but  is  prevented  from  falling  over  to  that  side  by  the 
support  of  the  stick,  w^hile  the  pelvis  and  hip-joint  of  the  paralyzed 
side  are  elevated  by  contraction  of  the  abductors  of  the  healthy  thigh, 
so  that  the  weight  is  taken  off  the  paralyzed  extremity.     When   the 


HEMIPLEGI.E.  479 

paralyzed  loAver  extremity,  say  the  right,  is  the  active  one,  the  line  of 
gravity  is  carried  over  to  a  slight  extent  to  that  side,  but  instead  of 
reaching  the  centre  of  the  paralyzed  foot  it  remains  midway  between  it 
and  the  end  of  the  stick,  so  that  the  weight  of  the  body  is  maintained 
partly  by  the  paralyzed  lower  extremity  and  partly  by  the  healthy  arm 
through  the  stick.  The  healthy  or  left  lower  extremity  is  now  moved 
forwards  a  step,  an  unusual  degree  of  flexion  of  the  thigh  upon  the 
body  taking  place  in  order  to  avoid  the  necessity  of  carrying  the  line 
of  gravity  too  far  to  the  paralyzed  side.  The  left  leg  now  becomes 
active  and  the  paralyzed  one  must  be  moved  forwards.  The  manner  in 
which  this  movement  is  executed  depends  upon  the  degree  of  paralysis 
and  of  muscular  rigidity  present.  If  the  paralysis  be  almost  complete, 
and  the  rigidity  not  great,  the  extremity  is  partly  swung  and  partly 
dragged  round  mainly  by  contraction  of  the  inward  rotators  of  the 
healthy  limb.  Contraction  of  these  muscles  causes  the  pelvis  to  rotate 
forwards  on  the  hip-joint  of  the  healthy  side,  and  consequently  the 
opposite  hip-joint,  dragging  after  it  the  paralyzed  leg,  is  moved  forwards. 
This  forward  movement  is  aided  by  a  further  elevation  of  the  right 
hip-joint  caused  by  contraction  of  the  abductors  of  the  opposite  thigh, 
and  sometimes  by  a  slight  backward  inclination  of  the  trunk  by  means 
of  which  the  distance  between  the  points  of  origin  and  insertion  of  the 
flexors  of  the  thigh  on  the  body  is  increased.  If  a  high  degree  of  con- 
tracture with  talipes  equinus  be  present,  the  paralyzed  lower  extremity 
is  moved  forwards  much  in  the  same  manner  as  has  already  been  de- 
scribed in  the  case  of  primary  lateral  spinal  sclerosis.  When  once  the 
weight  of  the  body  is  taken  ofl'  the  paralyzed  extremity  the  heel  becomes 
elevated,  and  the  toe  during  the  forward  movement,  which  takes  place 
in  a  semicircular  manner,  makes  a  characteristic  scraping  noise.  If 
tremors  or  choreoid  movements  be  present  in  the  paralyzed  lower  ex- 
tremity, the  hemiplegic  walk  may  become  modified  in  such  numerous 
ways  as  to  render  it  impossible  to  compare  the  different  varieties  which 
may  be  presented  in  a  single  description. 

b.   Combined  Tonic  and  Clonic  Spasms. 

In  the  combined  tonic  and  clonic  forms  of  post-hemiplegic  motor 
disorders  the  muscular  contractions  are  at  first  quite  like  those  which 
occur  in  late  rigidity,  but  after  a  time  some  of  the  muscles  implicated 
become  the  subjects  of  clonic  spasm.  The  combined  tonic  and  clonic 
spasms  of  hemiplegic  limbs  may  be  divided  into  (1)  intermittent  tremor 
and  (2)  choreiform  movements. 

(1)  Intermittent  tremor  is  produced  when  the  muscles  are  put  upon 
the   stretch  by  passive  movements  or  voluntary   effort.     This  kind  of 


480  THE    SPASMODIC    PARALYSES. 

tremor  is  similar  to  that  described  as  "spinal  epilepsy"  in  primary 
lateral  spinal  sclerosis,  and,  like  the  tremor  of  multiple  sclerosis,  it  is 
absent  during  repose.  The  muscles  of  hemiplegic  limbs  are  also  liable 
to  be  affected  with  fibrillary  contractions  similar  to  those  which  occur 
in  progressive  muscular  atrophy  and  amyotrophic  lateral  sclerosis,  but 
in  these  cases  it  is  probable  that  the  descending  changes  of  the  pyra- 
midal tract  have  extended  to  the  ganglion  cells  of  the  anterior  gray 
horns  of  the  cord. 

(2)  Choreiform  movements  of  the  extremities  may  either  precede  or 
follow  an  attack  of  hemiplegia,  the  former  being  named  pre-hemipJegie 
clwrea^  and  the  latter  post-hemiplegic  chorea.  In  pre-hemijiJegic  chorea 
the  patient  complains  of  a  feeling  of  numbness  and  feebleness  of  the 
extremities  of  one  side,  his  gait  becomes  hesitating  and  irregular,  and 
the  upper  extremity  of  the  affected  side  is  attacked  by  choreiform 
movements.  These  symptoms  may  continue  for  some  days,  when  com- 
plete hemiplegia,  usually  associated  with  hemiangesthesia,  is  either  sud- 
denly or  gradually  established.  Post-hemiplegic  chorea  occurs  in  par- 
tially but  never  in  completely  paralyzed  limbs,  and  usually  appears 
simultaneously  with  a  marked  diminution  of  the  paralytic  symptoms. 
The  clonic  spasms  become,  as  a  rule,  gradually  established  as  motor 
power  returns,  but  they  sometimes  appear  suddenly  during  a  voluntary 
effort  on  the  part  of  the  patient  to  move  the  paralyzed  limb.  Clonic 
spasms  appear  more  frequently  in  the  arm  than  in  the  leg,  and  when 
they  exist  in  both  they  ai'e  generally  more  severe  in  the  former  than  in 
the  latter,  while  if  they  exist  exclusively  in  the  leg,  the  arm  is  com- 
pletely paralyzed.  The  movements  affected  by  choreiform  spasms  are, 
in  their  increasing  order  of  frequency,  the  special  movements  of  the 
fingers  and  thumb,  pronation  and  supination  of  the  forearm,  extension 
and  flexion  at  the  elbow-joint,  and  movements  at  the  shoulder-joint. 
The  interossei  are  particularly  liable  to  be  affected  by  choreiform  spasm, 
and  consequently  the  movements  most  frequently  observed  consist  of 
varying  degrees  of  flexion  and  extension  at  the  metacarpo-phalangeal 
articulations,  associated  respectively  with  extension  and  flexion  at  the 
phalangeal  articulation.  The  movements  induced  by  these  spasms  are 
of  wider  range  than  those  of  the  hemiplegic  tremor,  resembling  in  this 
respect  the  movements  of  chorea  rather  than  the  tremors  of  primary 
lateral  spinal  sclerosis.  The  movements  are  disorderly  and  irregular, 
and  may  or  may  not  continue  during  repose ;  they  cease  during  sleep, 
and  become  much  aggravated  during  voluntary  efforts  to  perform  a 
definite  movement  with  the  affected  hmb,  such  as  that  of  raising  a  glass 
of  water  to  the  mouth.  Post-hemiplegic  chorea  of  adults  is  always 
accompanied  by  some   degree  of  antesthesia,  which   extends  over  the 


HEMIPLEGI^E.  481 

lateral  half  of  the  body  on  the  side  aiFected  with  spasm,  and  affects  all 
forms  of  cutaneous  and  muscular  sensibility  as  well  as  the  special  senses. 

c.   Clonic  Spas)iis. 
The  post-hemiplegic  motor  disorders  which  consist  of  clonic  spasms 
unaccompanied  by  tonic  contractions  of  the  muscles,  are  (1)  continuous 
or  remittent  tremor,    (2)   choreiform   movements    (athetosis),   and  (3) 
jerking  movements  on  voluntary  effort  (hemiataxia). 

(1)  Continuous  or  re7nittent  tremo?'  is  continuous  during  wakino- 
hours,  and  instead  of  being  exaggerated  by  voluntary  effort  like  the 
tremors  of  lateral  spinal  sclerosis  and  that  of  sclerosis  in  patches,  it 
may  be  diminished  or  arrested  for  a  short  time  by  a  voluntary  effort, 
being  in  this  and  other  respects  like  the  tremor  of  paralysis  agitans. 
The  tendon-reactions  are  not  sensibly  exaggerated  in  this  form  of 
tremor. 

(2)  Athetosis  is  a  condition  in  which  the  patient  is  unable  to  main- 
tain the  fingers  and  toes  in  fixed  positions.  The  fingers  and  toes  are 
maintained  in  continuous  slow  movement,  and  are  made  to  assume 
various  distorted  positions.  In  some  cases  these  movements  extend  to 
the  hand  and  foot,  and  occasionally  even  to  the  muscles  of  the  neck 
and  face.  No  motor  weakness  has  been  observed,  the  muscles  do  not 
become  tense  on  passive  movements,  and  the  tendon-reactions  are  not 
sensibly  exaggerated.  The  appearance  of  the  clonic  spasm  is  in  almost 
all  cases  preceded  by  a  distinct  attack  of  hemiplegia,  and  when  no 
decided  paralysis  can  be  ascertained  to  have  been  present,  the  historv 
of  the  case  shows  that  the  patient  has  suffered  from  an  attack  of  con- 
vulsions and  unconsciousness.  Hemianaesthesia  is  described  as  having 
been  present  in  a  considerable  number  of  the  reported  cases,  and  a 
certain  degree  of  numbness  of  the  affected  side  is  frequently  mentioned, 
Avliile  it  is  possible  that  diminution  of  sensibility  would  have  been  found 
in  all  cases  had  special  attention  been  directed  to  this  point.  The 
affected  extremity  usually  presents  vaso-motor  disturbances,  being  red 
or  livid,  moist,  and  colder  than  the  corresponding  extremity.  The 
affected  hand  or  foot  is  also  frequently  smaller  than  the  corresponding 
part  of  the  opposite  extremity,  although  the  muscles  affected  by  spasm 
may  undergo  a  certain  degree  of  hypertrophy.  The  electric  contrac- 
tility of  the  affected  muscles  varies  in  different  cases,  being  sometimes 
normal,  at  other  times  enfeebled  or  increased.  The  ligaments  and 
joints  of  the  affected  extremities  may  occasionally  be  found  considerably 
relaxed. 

(3)  Hemiataxia  consists  of  disorderly  or  incoordinate  movements  of 

the  limb  on  voluntary  effort,  coming  on  in  the  absence  of  paralysis, 

31 


482  THE    SPASMODIC    PARALYSES. 

permanent  rigidity,  or  spontaneous  spasm.  The  ataxic  movements 
become  most  marked  when  the  patient  is  asked  to  execute  a  complicated 
movement  with  the  afiected  limb  when  his  eyes  are  closed.  This  con- 
dition is  associated  with  a  slight  degree  of  anesthesia,  tactile  sensibility 
beino-  sometimes  found  diminished,  while  the  sensibility  to  pain  is 
normal. 

III.  SPECIAL  CONSIDERATION  OF  POST-HEMIPLEGIC  SPASMS  AS 
THEY  OCCUR  IN  INFANCY  (THE   SPASMODIC    PARALYSES  OF 
INFANCY). 
The  spasmodic  paralyses  of  infancy  may,  from  the  clinical  standpoint, 
be  divided  into  (1)  paralysis  of  hemiplegic  and  (2)  paralysis  of  para- 
plegic distribution,  and  in  addition  we  shall  consider  in  this  place  (3) 
the  cases  of  tonic  spasm  of  voluntary  muscles  described  by  Thomsen. 
It  is  possible  that  some  of  the   paraplegiie  of  infancy  are  of  spinal 
origin,   but   many  of  them   are  probably  to   be  regarded  as  bilateral 
hemiplegite  rather  than  as  true  hemiplegio?. 


1.  Spastic  Hemiplegle  of  Infancy. 

The  spastic  hemiplegite  of  infancy  may  be  divided  into  a,  acquired^ 
and  6,  coyigenital  spastic  liemiplegia?.  In  addition  we  shall  consider  in 
this  place  e,  double  athetosis. 

a.  Acquired  spastic  hemiplegia  of  infancy  dates  from  birth  or  begins 
at  any  time  between  that  date  and  four  or  five  years  of  age.  The  child 
is  unconscious  and  convulsed  for  the  first  few  days  after  birth  (as})hyxia 
neonatorum),  or  if  attacked  after  birth  it  is  suddenly  seized  with  con- 
vulsions and  unconsciousness  which  may  last  from  a  few  hours  to  a  few 
days.  The  convulsions  are  limited  to,  or  at  least  most  pronounced  on 
one  side  of  the  body,  and  this  side  becomes  subsequently  paralyzed. 
In  the  cases  Avhich  recover  the  hemiplegia  pursues  the  usual  course,  con- 
tractures become  established,  and  choreiform  movements  may  or  may 
not  make  their  appearance,  and  if  these  movements  once  make  their 
appearance  they  remain  permanent.  So  far,  then,  these  cases  present 
nothing  peculiar  except  that  the  disease  dates  from  childhood,  that  it  is 
ushered  in  by  convulsions  and  profound  unconsciousness,  and  that  the 
motor  paralysis  is  not  accompanied  by  hemiangesthesia.  But  as  the 
patient  advances  in  age  the  bones  of  the  paralyzed  limbs,  and  even  those 
of  the  paralyzed  half  of  the  face,  are  somewhat  arrested  in  their  develop- 
ment as  compared  with  the  corresponding  bones  of  the  healthy  side,  so 
that  the  former  are  found  to  be  smaller  in  all  their  dimensions  than  the 


THE    SPASMODIC    PARALYSES    OF    INFANCY.  483 

latter.  Each  of  the  long  bones  of  the  limbs  may  be  from  one-fourth  of 
an  inch  to  one  inch  shorter  than  the  corresponding  bones  of  the  healthy 
side,  and  even  the  clavicle  of  the  [laralyzed  side  may  be  from  one-fourth 
to  one-half  of  an  inch  shorter  than  the  opposite  clavicle.  The  diminu- 
tion in  size  of  the  half  of  the  face  may  extend  to  all  the  features,  in- 
cluding the  eyebrow,  eyelids,  half  of  the  nose,  the  cheek,  and  half  the 
mouth.  At  from  seven  to  fifteen  years  of  age  the  patient  is  attacked 
with  epileptic  convulsions,  which- recur  at  periodical  intervals  of  greater 
or  less  duration  during  the  rest  of  life.  These  convulsions  are  at  first 
limited  to  the  paralyzed  half  of  the  body,  and  they  are  not  always  ac- 
companied by  decided  loss  of  consciousness.  After  a  time,  however,  the 
convulsions  become  general,  but  even  then  they  often  retain  a  unilateral 
character  at  the  beginning  of  the  attack,  and  the  patient  usually  de- 
scribes a  unilateral  aura.  The  aura  is  often  described  as  a  numbness  or 
other  sensation  beginning  in  the  paralyzed  arm,  and  ascending  along 
the  arm  to  the  shoulder  and  then  to  the  side  of  the  face,  when  un- 
consciousness supervenes.  At  other  times  the  sensation  begins  in  the 
leg  and  ascends  successively  to  the  arm  and  side  of  the  head,  or  in  the 
side  of  the  face  and  descends  to  the  arm  and  leg.  The  intellectual 
faculties  almost  always  suffer  in  this  disease,  and  the  patient  is  usually 
more  or  less  idiotic,  but  in  some  cases  this  defect  of  intelligence  amounts 
only  to  a  certain  degree  of  imbecility,  which  becomes  established  only 
after  a  frequent  recurrence  of  the  epileptic  attacks. 

h.  Congenital  sjjastie  hemiplegia  presents  numerous  varieties,  and  all 
of  them  are  generally  associated  with  imbecility  or  idiocy.  In  some 
cases  the  paralysis  is  limited  to  one-half  of  the  body,  while  at  other 
times  both  sides  are  affected.  In  these  cases  there  is  absence  of  a 
history  of  convulsions  and  unconsciousness  occurring  at  birth  or  during 
childhood,  and  the  spasmodic  rigidity  of  the  affected  limbs  is  accom- 
panied, as  a  rule,  by  disorders  of  articulation,  wry  neck,  or  strabismus, 
while  the  skull  is  often  of  comparatively  small  size  and  unsymmetrical. 

(2.  Bilateral  athetosis  is  generally  of  congenital  origin,  and  is  always 
associated  with  more  or  less  idiocy,  and  of  articulatory  disorders,  while 
aphasia  is  sometimes  present.  The  muscles  of  the  face  are  more  liable 
to  be  implicated  in  the  spasm  of  the  bilateral  than  in  the  unilateral 
disease.  In  cases  of  bilateral  athetosis  sensory  disorders  have  not  been 
observed,  and  there  is  no  history  of  an  apoplectic  attack  or  convulsions 
having  occurred  during  infancy,  and  consequently  the  affection  is  most 
probably  of  congenital  origin. 


484 


THE    SPASMODIC    PARALYSES, 


2.  The  Spasmodic  Paraplegia,  of  Infancy. 

Children  are  liable  to  be  affected  with  a  spasmodic  paraplegia  from 
disease  of  the  vertebral  column  or  from  any  other  lesion  which  causes  a 
consecutive  transverse  myelitis ;  but  the  cases  which  are  under  discus- 
sion at  present  occur  at  birth,  or  are  of  congenital  origin.  In  this 
affection  the  muscles  of  the  lower  extremities  are  in  a  condition  of 
spasmodic  rigidity,  the  patellar  tendon-reactions  are  exaggerated,  and 
the  feet  are  generally  maintained  in  a  condition  of  talipes  equinus 
(Figs.  151  and  152)  oAving  to  the  predominance  of  the  actions  of  the 


Fig.  151. 


Fig.  152. 


muscles  of  the  calves,  while  the  gait  of  the  patient  is  like  that  of  lateral 
spinal  sclerosis.  The  upper  extremities  are  not  affected,  but  the  patient 
often  suffers  from  difficulties  of  articulation,  and  the  head  is  often  rather 
smaller  than  is  usual  in  healthy  children  of  the  same  age.  In  other 
cases  the  head  is  large  with  projecting  forehead,  showing  that  the  patient 
has  suffered  in  infancy  from  hydrocephalus  or  rickets.  When  the  spasm 
is  limited  to  the  lower  extremities  the  patient  is  often  quite  bright  and 


PARALYSES    FROM    FUNCTIONAL    DISEASE.  485 

intelligent,  and   feebleness   of  intellect  is   only  present  in  occasional 
cases,  but  the  patient  never  appears  to  sufier  from  epileptic  convulsions. 


IV.  MONOPLEGI^E. 

The  clinical  features  of  the  monoplegioe  do  not  require  lengthened 
description.  The  paralysis,  which  is  restricted  to  one  limb  or  to  certain 
groups  of  muscles  on  one  side  of  the  body,  is  accompanied  by  the  same 
kind  of  muscular  tension  and  excess  of  the  tendon-reactions  which  are 
met  with  in  hemiplegia.  The  clinical  varieties  most  usually  observed  are 
crural,  brachio-crural,  brachial,  brachio-facial,  facial,  labio-glosso,  and 
unilateral  oculo-motor  monoplegise. 

The  monoplegitfi  derive  their  chief  interest  not  so  much  from  their 
clinical  features  as  from  the  localization  of  the  lesions  which  give  rise 
to  them,  and  consequently  they  will  be  more  minutely  described  when 
we  come  to  discuss  the  morbid  anatomy  of  the  spasmodic  paralyses. 

Sensory  disorders  sometimes  accompany  the  paralyses  caused  by 
disease  of  the  cortex  of  the  motor  area  of  the  brain.  The  tactile  sen- 
sibility and  the  muscular  sense  are  specially  liable  to  be  diminished  in 
the  paralyzed  limbs  in  cortical  disease.  Vaso-motor  and  trophic  dis- 
orders, consisting  of  elevation  of  the  temperature  of  the  paralyzed  limbs 
and  acute  bedsores,  have  also  been  observed  in  cases  of  disease  of  the 
cortex  of  the  brain,  but  these  symptoms  do  not  possess  any  value  in 
determining  the  localization  of  the  lesion. 


V.   PARALYSES   FROM   FUNCTIONAL   DISEASE. 

1,  Post-epileptic  Paralysis. 

Attacks  of  unilateral  epilepsy  are  always  followed  by  a  temporary  or 
permanent  paralysis  of  the  convulsed  limbs,  which  is  attended  by  some 
degree  of  exaggeration  of  the  tendon-reactions,  showing  that  this  form 
of  paralysis  belongs  to  the  spasmodic  or  cerebro-spinal  variety.  The 
general  convulsions  of  idiopathic  epilepsy  are  followed  by  a  general 
resolution  of  the  limbs  which  is  not  usually  spoken  of  as  a  paralysis 
because  all  the  limbs  are  affected 'in  an  equal  degree.  This  muscular 
feebleness  sometimes  predominates  on  one  side  of  the  body  or  in  one 
limb,  and  then  it  is  recognized  to  be  of  a  distinctly  paralytic  nature, 
and  there  can  be  little  doubt  that  the  general  muscular  relaxation  which 
follows  an  epileptic  attack  ought  also  to  be  regarded  as  a  paralysis. 


486  THE    SPASMODIC    PARALYSES. 


2.  Hysterical  Paralysis. 

Partial  or  complete  loss  of  muscular  power  is  a  frequent  symptom  of 
hysteria.  The  loss  of  motor  power  may  begin  with  mere  weakness  and 
heaviness  of  the  limbs,  and  these  symptoms  may  gradually  increase  until 
complete  paralysis  is  established,  but  at  other  times  complete  paralysis 
is  suddenly  established  after  a  hysterical  attack.  The  paralysis  may 
assume  the  form  of  paraplegia,  hemiplegia,  monoplegia,  or  it  may  be 
limited  to  one  or  more  motor  nerves  or  to  particular  branches  of  a  nerve. 

Hysterical  hemiplegia  often  supervenes  after  an  attack  of  convulsions 
Avith  partial  loss  of  consciousness,  so  that  in  its  mode  of  onset  as  well  as 
in  its  clinical  features  it  resembles  the  hemiplegia  which  results  from  an 
apoplectic  seizure,  and  the  fact  that  contractures  become  developed  in 
the  former  as  well  as  in  the  latter,  renders  the  similarity  between  them 
still  more  striking. 

In  some  cases  the  contracture  appears  simultaneously  with  the  paral- 
ysis, while  in  other  cases  a  paralysis  with  flaccidity  is  established  and 
continues  for  some  tinie  and  then  contracture  develops  gradually  or 
suddenly  after  a  fresh  attack.  In  the  upper  extremity  the  forearm, 
hand,  and  fingers  are  spasmodically  flexed,  and  the  muscles  may  be  so 
rigid  that  it  is  impossible  to  obtain  complete  extension  or  to  increase  the 
flexion.  The  lower  extremity  is  strongly  extended  upon  the  pelvis  and 
the  leg  upon  the  thigh,  while  the  foot  assumes  the  position  of  extreme 
talipes  equino-varus.  In  hysterical  paraplegia  both  lower  extremities 
assume  the  position  just  described,  and  the  knees  are  drawn  inwards 
and  strongly  pressed  against  each  other  by  contraction  of  the  adductors 
of  the  thighs.  In  hysterical  paralysis  with  contracture,  tremor  is  some- 
times observed  on  attempting  any  movement.  The  patellar  tendon- 
reactions  are  often  exaggerated  and  even  ankle-clonus  may  sometimes 
be  elicited,  these  being  the  symptoms  which  are  so  characteristic  of  the 
paralysis  which  results  from  sclerosis  of  the  lateral  columns  of  the  cord. 
Hysterical  hemiplegia  diff'ers  from  hemiplegia  due  to  organic  disease  of 
the  brain  in  the  following  respects :  It  is  usually  accompanied  by  hemi- 
anaesthesia,  and  by  emotional  disturbances,  and  other  well-marked 
hysterical  phenomena  ;  the  paralysis  is  scarcely  ever  complete,  the  face 
and  tongue  almost  never  being  aftected  ;  the  leg  is  generally  more  para- 
lyzed than  the  arm,  and  the  diminution  of  motor  power  is  liable  to 
sudden  variations  of  intensity  under  the  influence  of  diff"erent  emotions. 
Hysterical  paralysis  may  be  distinguished  from  atrophic  paralyses  by 
the  facts  that  in  it  the  electrical  reactions  of  the  muscles  remain  normal, 
and  the  muscles  do  not  undergo  active  wasting.     These  tests,  however. 


PARALYSES    FKOM    FUNCTIONAL    DISEASE.  487 

fail  in  distinguishing  hysterical  paralysis  from  Landry's  paralysis,  and 
as  a  matter  of  history  the  latter  has  freijuently  been  mistaken  for 
hysterical  paralysis.  The  most  trustworthy  diagnostic  sign  between 
the  two  affections  is  afforded  by  the  patellar  tendon-reaction,  which  is 
generally  exaggerated  in  hysterical  paralysis  and  absent  in  Landry's 
paralysis. 

For  purposes  of  diagnosis  the  student  should  pay  particular  attention 
to  the  features  Avhich  distinguish  the  gait  of  a  person  suflFering  from 
hysterical  paralysis  and  that  of  one  suffering  from  a  spasmodic  paralysis 
caused  by  organic  disease.  In  organic  spasmodic  paralysis,  whether  of 
the  hemiplegic  or  paraplegic  variety,  when  the  affected  extremity  is  to 
be  moved  forward  in  walking  the  heel  becomes  strongly  elevated  and 
the  toes  depressed ;  the  necessary  elevation  to  clear  the  toes  off  the 
ground  is  obtained  chiefly  by  elevation  of  that  side  of  the  pelvis ;  and 
the  foot  is  projected  forward  by  a  movement  of  circumduction,  the  toes 
making  a  scraping  noise  on  the  ground.  In  hysterical  paralysis  there 
is  little  or  no  elevation  of  the  heel  or  depression  of  the  toes  during  the 
forward  movement  of  the  foot ;  the  necessary  elevation  to  clear  the  foot 
off  the  ground  is  obtained  by  flexion  of  the  limb  at  the  hip-  and  knee- 
joints,  and  consequently  rotation  of  the  pelvis  is  not  a  marked  feature 
of  the  walk ;  there  is  no  movement  of  circumduction,  and  the  toes  do 
not  scrape  the  ground.  In  hysterical  paralysis  the  foot  is  maintained 
throughout  the  whole  forward  movement  at  right  angles  with  the  leg, 
and  as  it  is  made  to  glide  forwards  the  sole  is  held  close  to  and  almost 
parallel  with  the  ground. 

The  relative  feebleness  of  the  extensors  of  the  toes  in  comparison 
with  those  of  the  heels  in  spastic  paralysis  from  organic  disease,  may 
be  tested  in  another  way.  If  the  patient  be  placed  with  her  back 
against  a  wall,  so  as  to  prevent  her  from  inclining  the  body  forwards,  it^ 
will  be  found  that  when  she  attempts  to  elevate  the  toes  a  spasm  of  the 
muscles  of  the  calf  supervenes,  which  fixes  the  anterior  part  of  the  foot  still 
further  to  the  ground,  but  in  hysterical  paralysis  the  patient  may  often, 
although  not  always,  be  coaxed  to  elevate  her  toes  just  like  a  healthy 
person,  and  even  when  she  refuses  to  make  the  necessary  effort  it  will 
be  found  that  the  anterior  part  of  the  foot  does  not  become  so  strongly 
fixed  to  the  ground  as  in  organic  paralysis.  In  organic  spasmodic 
paralysis  of  the  lower  extremities  the  reflex  of  the  sole  is  exaggerated, 
while  it  is  often  absent  when  the  paralysis  is  hysterical.  In  spasmodic 
paralysis  of  the  lower  extremities  from  organic  disease  the  patient  fixes 
her  eyes  steadily  on  the  ground,  but  the  hysterical  patient  either  looks 
about  her,  or,  while  pretending  to  look  at  the  ground,  she  casts  stealthy 


488  THE    SPASMODIC    PARALYSES. 

glances  from  tlie  corners  of  her  eyes  to  see  what  effect  she  is  producing 
on  the  surrounding  observers. 

Of  the  paralyses  which  occur  in  the  region  of  distribution  of  par- 
ticular nerves,  hysterical  aphonia  is  probably  the  most  frequently  met 
with.  In  hysterical  aphonia  the  loss  of  voice  appears  suddenly  after 
some  mental  excitement,  and  may  disappear  with  e(pial  celerity,  and  it 
is  not  attended  by  a  persistent  cough  like  laryngitis.  A  laryngoscopic 
examination  reveals  the  signs  of  paralysis  of  the  glottis,  sometimes  on 
one  and  at  other  times  on  both  sides.  DiflRculty  of  moving  the  tongue 
is  sometimes  associated  with  the  laryngeal  paralysis,  and  the  patient  is 
no  longer  able  to  articulate  in  a  Avhisper,  but  has  to  resort  to  pantomime 
in  order  to  make  herself  understood.  Paralysis  of  the  muscles  of  the 
pharynx  and  oesophagus  is  not  an  uncommon  symptom  of  hysteria, 
and  swallowing  then  becomes  difficult  or  impossible.  In  such  a  case 
the  oesophageal  tube  passes  into  the  stomach  without  encountering  any 
obstruction.  Inspiratory  dyspnoea  is  a  frecjuent  symptom  of  hysteria, 
and  it  is  possible  that  it  is  sometimes  caused  by  a  temporary  paralysis  of 
the  diaphragm.  Paralysis  of  the  muscular  coat  of  the  stomach  is  partly 
the  cause  and  partly  the  effect  of  the  general  tympanites  which  is  so 
frequently  met  with  in  hysterical  patients.  The  obstinate  constipation 
which  is  so  frequent  a  s^'mptom  of  hysteria  is  probably  caused  by 
paralysis  of  the  muscular  coat  of  the  l)owel.  Retention  of  urine  is 
common  in  hysteria,  but  it  is  not  often  of  paralytic  origin.  Hysterical 
women  have  been  known  to  drop  down  dead  after  a  great  shock,  and 
in  these  cases  death  is  doubtless  caused  by  paralysis  of  the  heart. 
Various  phenomena  occur  in  hysterical  patients  from  paralysis  of  the 
vaso-motor  nerves.  The  excessive  menstruation,  and  even  the  haemop- 
tysis and  haematemesis  which  are  occasionally  observed  are  most  prob- 
ably caused  by  paralysis  of  vaso-motor  nerves. 


3.  Toxic  Paralyses. 

Various  poisons  give  rise,  as  we  have  already  seen,  to  paralysis  by 
causing  organic  disease  of  the  nervous  system.  Clironic  poisoning  l)y 
lead  and  by  alcohol,  as  well  as  the  poison  of  diphtheria,  cause  a  paral- 
ysis which  we  have  reasons  for  believing  is  due  to  a  progressive  multi- 
ple neuritis,  and  it  is  very  probable  that  arsenic  and  many  other  metallic 
salts  act  in  a  similar  manner.  Other  poisons  cause  paralysis  by  induc- 
ing a  molecular  or  functional  change  in  peripheral  nerves,  such  as 
curara,  which  acts  upon  the  intramuscular  nerve-endings,  and  atropine, 
which  paralyzes   the  terminations  of  the  vagi  and   the  nerves  which 


MOEBID    ANATOMY.  489 

supply  the  ciliary  muscle  and  the  sphincter  of  the  iris.  Some  of  the 
methyl  compounds  of  conium  produce  parah^sis  by  depressing  the  irrita- 
Itility  of  the  gray  matter  of  the  spinal  cord  and  of  the  motor  nerves. 
This  subject  is,  however,  so  wide  that  were  it  to  l)e  fully  discussed  we 
should  have  to  go  over  nearly  the  whole  field  of  toxicology. 

Some  poisons  appear  to  act  on  the  fibres  of  the  pyramidal  tracts. 
Cases  of  spasmodic  spinal  paralysis  investigated  by  Dr.  Brunelli  render 
it  probable  that  the  symptoms  were  caused  by  a  species  of  vetch — 
lathyrus  cicera — which  was  used  by  the  patients  as  a  chief  article  of 
diet. 

A  case  I  saw  a  short  time  ago  along  with  my  friend,  Dr.  Niven, 
would  seem  to  show  that  the  symptoms  of  spastic  spinal  paralysis  may 
be  caused  by  malaria.  The  patient  came  home  an  invalid  from  South 
America  some  weeks  before  I  saAv  him.  When  I  examined  him  he  was 
suffering  from  the  usual  symptoms  of  a  primary  lateral  sclerosis,  con- 
sisting of  stiiFness  and  feebleness  of  the  lower  extremities,  muscular 
tension,  exaggerated  patellar  tendon-reaction,  ankle-clonus,  and  decided 
spastic  gait.  Iodide  of  potassium  was  ordered,  but  the  symptoms  did 
not  improve  much.  Dr.  Xiven  uoav  ascertained  that  the  patient  was 
suffering  from  well-marked  attacks  of  airue,  and  he  was  accordingly 
treated  with  large  doses  of  quinine,  and  not  only  did  the  febrile  symp- 
toms disappear,  but  the  spinal  symptoms  also  improved  rapidly,  and  the 
patient  left  for  South  America,  two  months  afterwards,  with  scarcely  a 
trace  of  the  stiffness  or  exaggei'ated  tendon-reactions  of  the  lower 
extremities  to  be  detected. 


MORBID  ANATOMY. 

I.  Paraplegia. 

Some  pathologists  doubt  whether  such  a  disease  as  a  primary  sym- 
metrical sclerosis  of  the  lateral  columns  has  yet  been  proved  to  exist. 
Cases  have  been  reported  in  which  the  symptoms  attributed  to  primary 
lateral  sclerosis  were  present  during  life,  but  which  proved  on  post- 
mortem examination  to  have  been  examples  of  sclerosis  in  patches,  or 
tumor  of  the  medulla  oblongata,  or  of  the  cerebellum.  The  most 
notable  case  of  primary  lateral  sclerosis  so  far  reported  is  that  of  a 
man  under  the  care  of  my  colleague,  Dr.  Morgan,  in  the  Manchester 
Royal  Infirmary.  The  patient  died  from  some  intercurrent  disease, 
and  Dr.  Dreschfeld,  who  conducted  the  microscopical  examination, 
■  found  symmetrical  sclerosis  of  the  pyramidal  tracts  of  the  spinal  cord 


490 


THE    SPASMODIC    PAKALYSES. 


from  the  medulla  oblongata  to  the  conus  medullaris,  and,  with  the  ex- 
ception of  slight  atrophy  of  the  ganglion  cells  of  the  anterior  gray 
horns,  an  entire  absence  of  any  other  lesion.  The  presence  of  some 
atrophy  in  the  ganglion  cells  in  this  case  has  led  Westphal  to  suggest 
that  it  was  an  example  of  amyotrophic  lateral  sclerosis,  but  having 
watched  the  symptoms  during  life,  and  examined  sections  of  the  spinal 
cord,  I  do  not  concur  in  this  view.  A  secondary  symmetrical  sclerosis 
of  the  lateral  columns  is  caused  by  all  transverse  lesions  of  the  spinal 
cord.  Transverse  and  compressive  myelitis  are  followed  by  a  descend- 
ing sclerosis  of  the  antero-lateral  pyramidal  tracts  below  the  level  of 
the  lesion,  and  an  ascending  sclerosis  of  the  columns  of  Goll  and  direct 
cerebellar  tracts,  but    these  conditions   have  already  been   sufficiently 

described. 

Fig.  153. 


Transverse  Section  of  the  Medulla  Oblojigata  on  a  level  with  the  middle  of  the  Nucleus  of 
THE  Hypoglossal.  (From  Charcot.) 
E,  R',  median  raphe  ;  A,  B,  represents  the  normal  condition,  and  A',  B',  the  parts  as  they  appear  in 
amyotrophic  lateral  sclerosis  ;  C,  C,  the  floor  of  the  fourth  ventricle ;  V,  a  vessel  which  bounds  the 
nucleus  of  the  hypoglossal  anteriorly  and  externally  ;  D,  fasciculus  teres?  and  D',  the  corresponding  part 
on  the  diseased  side  ;  A,  healthy  nucleus  of  the  hypoglossal ;  and  A',  the  diseased  nucleus.  B,  the  healthy 
nucleus  of  the  pneumogastric  nerves ;  and  B',  the  nucleus  on  the  diseased  side,  which  is  seen  not  to  be 
much  affected. 

Morbid  Anatomy. — In  amyotrophic  lateral  sclerosis  Charcot  and 
others  have  proved  the  presence  of  symmetrical  sclerosis  of  the  pyra- 
midal tracts  of  the  antero-lateral  columns  of  the  cord,  and  of  the 
anterior  pyramids  of  the  medulla  oblongata,  along  with  degenerative 
atrophy  of  the  anterior  gray  horns  and  of  the  motor  nuclei  in  the 
medulla  oblongata,  and  loss  of  the  motor  ganglion  cells.  The  condi- 
tion of  the  bulbar  nuclei  is  represented  in  Fig.  153,  borrowed  from 


MORBID    ANATOMY. 


491 


Charcot,  the  diseased  nuclei  being  shown  to  the  left  of  a  fictitious  line 
(R  E/),  and  the  healthy  one  for  the  sake  of  comparison  to  the  right  of 
that  line.  The  part  which  Charcot  calls  the  fasciculis  teres  really  con- 
sists of  a  group  of  small  cells  which  I  have  called  the  external  acces- 
sory nucleus  of  the  facial.  It  is  seen  to  be  diseased  on  the  left  side 
(D'")  of  the  figure. 

II.  Hemiplegia. 


1.   Ordinary  Hemi'plegia. 

The  fibres  which  issue  from  the  motor  ganglion  cells  of  the  cortex 
form  separate  bundles  in  the  centrum  semiovale,  and  descending  in  the 
corona  radiata  come  together  in  the  internal  capsule.  Speaking  some- 
what broadly,  it  may  be  said  that  the  fibres  of  the  middle  third  of  the 
posterior  segment  of  the  internal  capsule  (Fig.   154,  P)  are  concerned 

Fig.  154. 


Horizontal  Section  of  the  Basal  Ganglia  and  Internal  Capsule  in  an  embrto  of  nine  months. 
KC,  Caudate  nucleus ;   TU,  Optic  thalamus ;  IX,  Island  of  Reil ;  //,  III,  Second  and  third  segments  of 
the  lenticular  nucleus ;  ps,  Sensory  peduncular  tract  ;   P,  Fundamental,  and  P',  Mixed  portion,  and  p, 
Geniculate  fasciculus  of  the  pyramidal  tract.;  c.  Anterior  segment  of  the  internal  capsule. 

in  regulating  the  actions  of  the  trunk,  lower  extremities,  and  probably 
the  general  actions  of  the  upper  extremities;  that  the  fibres  of  the 
anterior  third  of  the  posterior  segment  (Fig.  154,  P')  are  concerned  in 


492 


THE    SPASMODIC    PARALYSES. 


regulating  the  special  movements  of  the  hand  as  an  organ  of  prehen- 
sion, and  probably  also  the  movements  of  the  rotation  of  the  head  and 
neck  along  Avith  the  associated  ocular  movements;  and  that  the  fibres 
of  the  knee  (Fig  154,  P)  and  the  adjoining  part  of  the  anterior  segment 
of  the  capsule  are  concerned  in  the  regulation  of  the  movements  of  facial 
expression,  articulation,  and  the  most  special  movements  of  the  hand, 
such  as  those  of  writing.  The  posterior  third  of  the  posterior  segment 
of  the  capsule  contains  the  sensory  conducting  paths,  and  injury  of  these 


Cls- 


Vertical  Section  of  the  Bkain  a  little  behind  the  Knee  of  the  Internal  Capsule,  showing  the 

EFFECTS   OF   RUPTURE   OF  THE   LENTICULO-STRIATE   ARTERY.       (Modified  from  CHARCOT.) 

NO,  Head,  and  NC,  Tail  of  the  caudate  nucleus ;  Ch,  Chiasma,  NL,  Lenticular  nucleus ;  IK,  Internal 
capsule;  Cls,  Claustrum ;  1,  The  most  frequent  position  in  wliich  the  lenticulo-striate  artery  is  ruptured; 
1',  1",  V",  Progressive  extension  of  the  hcmorrliage  producing  compression  and  rupture  of  the  fibres  of 
the  pyramidal  tract  (liemiplegia) ;  2,  Primary  focus  in  the  internal  capsule ;  2',  2",  2'",  Successive  extension 

of  the  clot. 

causes  hemiansesthesia.  Of  all  the  arteries  of  the  brain,  the  lenticulo- 
striate  artery  is  the  one  most  liable  to  rupture.  If  the  hemorrhage  be 
small,  it  may  lodge  between  the  external  cap.sule  and  the  lenticular  nucleus 
and  give  rise  to  no  symptoms.  The  vessel,  however,  is  a  comparatively 
large  one,  and  the  hemorrhage  usually  extends  beyond  these  limits.  It 
is  sometimes  directed  upwards  between  the  external  capsule  and  the 
lenticular  nucleus,  and  it  may  then  extend  for  a  considerable  distance 
with  the  centrum  ovale,  the  fibres  of  the  internal  capsule  become  rup- 


MORBID    ANATOMY.  493 

tared  at  tlie  point  -where  they  form  the  foot  of  the  corona  radiata,  and  the 
hemorrhage  may  then  be  so  extensive  as  to  extend  upwards  to  the 
summits  of  the  ascending  frontal  and  parietal  convolutions,  and  out- 
wards so  as  to  compress  the  Island  of  Reil,  but  the  external  capsule  is 
only  rarely  ruptured.  At  other  times  the  hemorrhage  is  directed 
inwards  through  the  gray  matter  of  the  lenticular  nucleus,  and  if  it 
remain  limited  to  the  nucleus  the  patient  will  recover  almost  completely 
from  the  hemiplegia  which  follows  the  attack.  But  if  the  clot  is  large 
enough  to  rupture  the  internal  capsule  (Fig.  155, 1"),  the  fibres  below  the 
seat  of  the  lesion  undergo  descending  sclerosis,  and  the  paralysis  remains 
more  or  less  permanent.  In  descending  sclerosis  the  morbid  changes 
are  observed  in  the  middle  third  of  the  crusta,  the  longitudinal  bundles 
of  the  pons,  the  anterior  pyramid  of  the  medulla  oblongata  and  the 
column  of  Tiirck  on  the  side  of  the  lesion,  and  in  the  lateral  column 
of  the  cord  on  the  side  opposite  to  the  lesion.  In  some  cases  a  large 
hemorrhage  may  I'upture  into  the  lateral  ventricle  and  then  death  takes 
place  in  a  few  hours. 

Rupture  of  the  lenticulo-striate  artery  gives  rise  to  a  hemiplegia  in 
which  the  arm  is  more  paralyzed  than  the  leg  or  face.  If  one  of  the  an- 
terior branches  of  the  artery  is  the  seat  of  rupture  the  anterior  segment 
of  the  capsule  may  be  injured  to  a  greater  degree  than  the  posterior  seg- 
ment, and  then  paralysis  of  the  face  predominates.  Hemorrhage  of 
the  caudate  nucleus  may,  by  pressing  on  the  internal  capsule,  cause  a 
hemiplegia  in  which  the  face  is  more  paralyzed  than  the  arm  or  leg. 

2.  Hemiplegia  and  Hemiancesthesia. 

Hemorrhage  of  the  lenticulo-optic  artery  (Fig.  154)  impinges  against 
the  posterior  part  of  the  posterior  segment  of  the  capsule,  and  causes 
hemiplegia  in  which  the  leg  is  more  paralyzed  than  the  arm  or  face, 
and  which  is  accompanied  by  hemiansesthesia. 

3.  Hemiplegia^  Hemiancesthesia,  and  Hemianopsia. 

The  internal  capsule  may  be  injured  by  lesions  of  the  optic  thalamus. 
Hemorrhage  of  the  posterior  internal  optic  artery,  if  small,  does  not 
give  rise  to  any  definite  symptoms,  but  if  large  it  ruptures  into  the 
lateral  ventricles  and  causes  death  in  a  short  time.  Hemorrhage  from 
the  posterior  external  optic  artery  does  not  usually  give  rise  to  pro- 
nounced hemiplegia,  but  it  causes  hemiansesthesia  of  the  opposite  side 
from  injury  of  the  sensory  peduncular  fibres  of  the  optic  radiations  of 
Gratiolet.  When  the  lesion  occurs  in  the  pulvinar  the  external  geni- 
culate body  is  apt  to  be  implicated  and  then  bilateral  hemianopsia  of  the 


494 


THE    SPASMODIC    PARALYSES. 


opposite  side  results  along  with  hemiplegia  and  hemianaesthesia,  and  the 
same  symptoms  have  occasionally  been  observed  when  the  lesion  is 
situated  too  far  forwards  to  injure  the  external  geniculate  body. 

When  a  large  hemorrhage  occurs  in  the  area  of  distribution  of  the 
posterior  external  optic  artery,  the  effused  blood  ruptures  the  posterior 
part  of  the  internal  capsule,  either  wholly  or  partially,  and  makes  its 
way  inwards  and  backwards  so  as  to  tear  up  a  considerable  portion  of 
the  anterior  tubercle  of  the  corpora  quadrigemina.     It  is  in  such  cases 

Fio.  156. 


Cls 


Vertical  Section  of  the  Brain  ox  a  level  with  the  Posterior  Part  of  the  Internal  Capsule, 

SHOWING   THE   EFFECTS   OP   RUPTURE   OF  THE   LENTICULO-OPTIC  ARTERY  (hEMIAN.ESTHESIA).      (Modified  from 

Charcot.) 

NC,  NC,  Head  and  Tail  of  the  caudate  nucleus ;  NL,  Lenticular  nucleus ;  TH,  Optic  thalamus ;  Cls, 
Claustrum  ;  1,  Primary  focus  in  the  posterior  part  of  the  external  capsule  (hemiansesthesia) ;  1',  1",  1'", 
Progressive  extension  of  the  primary  focus  causing  compression  or  destruction  of  the  internal  capsule ; 
2,  Primary  focus  in  the  internal  capsule  (hemian;esthesia)  ;  2',  2",  2'",  Successive  extension  of  the  focus. 

that  the  hemiplegia  and  hemianresthesia  with  the  peculiar  disorder  of 
the  movements  of  the  eyeballs  already  described  have  been  observed. 
The  clot  in  these  cases  is  only  separated  from  the  general  ventricular 
cavity  by  a  thin  layer  of  tissue,  consisting  chiefly  of  the  ependyma  of 
the  ventricle,  and  under  such  circumstances  it  is  very  probable  that  some 
serous  exudation  will  take  place  into  the  ventricles.  The  passage  of 
this  fluid  through  the  aqueduct  of  Sylvius  into  the  fourth  ventricle  may 
possibly  explain  the  presence  of  Cheyne-Stokes  respiration  in  these  cases. 


MORBID    ANATOMY, 


495 


4.    Crossed  or  Alternate  Hemiplegia. 

When  the  lesion  is  situcated  in  the  crus  cerebri  the  fibres  of  the  third 
nerve  in  their  passage  from  the  nucleus  to  their  point  of  emergence 
are  damaged,  while  the  fibres  of  the  pyramidal  tract  in  the  middle  third 
of  the  crusta  are  ruptured  or  compressed  (Fig.  157,  p).  The  conse- 
quences of  a  lesion  in  this  position  are  that  the  muscles  innervated  by 
the  third  nerve  are  paralyzed  on  the  side  of  the  lesion,  while  the  limbs 


sf-i^:  ^rc<  ^  /?^jl'--:v--  i^^-^;'^:- -^ti^;?>pi^  Sf 

\--^'  -^.-^V  ':••■•?.<'•■>.  >vi«»3>>-:-^  -~  ■  'r'\^^y 


Crura  Cerebri.  Transverse  Section  of  the  Crura  Cerebri  on  a  level  with  the  anterior  pair 
OF  the  Corpora  Quadrigemina  :  from  a  nine-months  human  embryo.  The  dark  portions  represent 
Medullated  Fibres. 

s,  Aqueduct  of  Sylvius  ;  g,  q',  Anterior  pair  of  Corpoi-a  Quadrigemina;  pf,  pf,  Fasciculi  of  Medullated 
Fibres  proceeding  to  the  anterior  pair  of  Corpora  Quadrigemina;  L,  L',  Posterior  Longitudinal  Fasciculi ; 
V,  V,  portions  of  these  Fasciculi  which  join  the  posterior  commissure  of  the  third  ventricle  ;  g,  g',  External 
Geniculate  Bodies  ;  af,  af.  Anterior  portion  of  Fillet ;  n,  n',  Substantia  Nigra ;  R,  R',  Red  Nuclei ;  p,  p', 
Pyramidal  Tract ;  c,  c',  Crustae  ;  3,  3',  Third  pair  of  nerves ;  x,  Decussation  in  front  of  the  Aqueduct  of 
Sylvius,  which  is  part  of  the  interlacement  of  the  Tegmentum. 

are  paralyzed  on  the  opposite  side  of  the  body,  because  the  pyramidal 
tract  is  injured  above  the  crossing  of  the  fibres  of  the  two  sides  in  the 
medulla  oblongata. 

If  the  lesion  is  situated  in  the  lower  part  of  the  lateral  half  of  the 
pons  there  is  well-marked  facial  paralysis  on  the  side  of  the  lesion,  and 
a  more  or  less  complete  motor  and  sensory  paralysis  of  the  limbs  on  the 
opposite  side.     In  order  to  account  for  these  phenomena  it  is  necessary 


496 


THE    SPASMODIC    PARALYSES. 


to  assume  that  the  fibres  of  the  pyramidal  tract,  which  connect  the 
cortex  of  the  opposite  hemisphere  with  the  nucleus  of  the  facial  nerve 
in  the  upper  part  of  the  medulla,  cross  over  about  the  middle  of  the 
pons,  as  represented  in  Fig.  158. 


5 — V- 


L,  Left, 
if,  Right. 
P,  Pons. 
M,  Medulla  oblongata. 


(From  XoTiiNAGEi..) 

DP,  Decussatio  pyramidiini. 

E,  Nerve  fibres  for  the  extremities. 

F,  Fibres  destined  for  the  facial  nerve. 
X,  Lesion  in  the  upper  part  of  the  pons. 


y,  Lesion  in  the  lower  part  of  the  pons. 


5.  IlemijAegic  and  Post-hemiplegic  Spasn^s. 

It  is  in  the  area  of  distribution  of  the  posterior  external  optic  artery 
that  the  lesion  has  almost  always  been  found  in  cases  of  post-hemiplegic 
chorea.  The  lesions  which  have  been  found  in  hemichorea  are  the 
remains  of  old  hemorrhages,  or  softening  from  occlusion  of  the  posterior 
external  optic  artery,  although  choreiform  movements  have  occasionally 
been  observed  during  the  groAvth  of  tumors  in  this  region.  It  is  evident, 
therefore,  that  the  symptoms  depend  not  upon  the  nature  of  the  lesion, 
but  upon  its  localization.  In  three  cases  of  unilateral  athetosis  observed 
by  Charcot  the  lesion  was  situated  in  the  posterior  extremity  of  the 
optic  thalamus  in  one,  the  posterior  extremity  of  the  caudate  nucleus  in 
the  second,  and  the  posterior  part  of  the  corona  radiata  in  a  third.  In 
a  case  observed  by  Landouzy  an  old  focus  of  softening  was  found  in 
the  portion  of  the  lenticular  nucleus  which  adjoins  the  internal  capsule, 
and  in  one  reported  by  Ringer  a  focus  of  softening  Avas  found  in  the 
posterior  part  of  the  lenticular  nucleus  near  to  the  internal  capsule.  In 
a  case  observed  by  Gnauck  the  coexistence  of  sensory  disturbances  in 
the  region  of  distribution  of  the  fifth  nerve  on  the  side  opposite  to  the 
spasmodic  movements  rendered  it  probable  that  the  lesion  was  situated 


MORBID    AXATOMY.  497 

in  the  lateral  half  of  the  pons.  It  is,  therefore,  probable  that  the  lesion 
in  athetosis  may  occupy  different  positions  in  the  vicinity  of  the  pyra- 
midal tract.  In  all  the  cases  hitherto  examined  after  death  the  posi- 
tions occupied  by  the  lesion  render  it  pro))able  that  the  fibres  of  the 
pyramidal  tract  are  never  completely  ruptured  and  that  there  are  no 
descending  changes  in  the  coixl,  but  the  fibres  of  the  tract  are  likely  to 
haA'e  suffered  partial  damage. 


III.  Special  Consideration  of  Lesions  of  the   Pyramidal 
Tracts  as  they  Occur  in  Infants. 

1.  Unilateral  or  JJiffused  Atropliy  of  the  Brain. — The  lesions  in 
the  acquired  spastic  hemiplegia  of  infancy  have  been  found  situated  in 
the  motor  area  of  the  cortex  of  the  brain.  The  primary  lesion  appears 
to  consist  of  a  local  hemorrhage,  softening  from  occlusion  of  a  vessel 
or  a  local  encephalitis.  As  a  general  rule  q,  puckered  cicatrix  forms  at 
the  seat  of  the  primary  lesion,  and  the  surrounding  portion  of  the 
cortex  undergoes  a  diff"used  sclerosis  with  retraction,  so  that  the  motor 
area  of  the  cortex  of  that  side  becomes  much  smaller  than  the  corre- 
sponding area  of  the  opposite  hemisphere,  and  consequently  such  cases 
have  been  named  unilateral  atrophy  of  the  brain.  In  addition  to  the 
changes  occurring  in  the  cortex,  the  fibres  of  the  jtyramidal  tract  con- 
nected Avith  the  diseased  area  undergo  a  descending  sclerosis,  and  con- 
sequently the  crusta  of  the  crus  cerebri,  the  longitudinal  fibres  of  the 
pons,  and  the  anterior  pyramid  of  the  medulla  oblongata  on  the  side  of 
the  lesion  are  found  atrophied,  while  a  microscopical  examination  reveals 
a  patch  of  sclerosis  in  the  lateral  column  of  the  spinal  cord  on  the  side 
opposite  to  the  lesion.  In  a  considerable  number  of  the  reported  cases 
the  lateral  lobe  of  the  cerebellum  on  the  opposite  side  to  that  of  the 
cerebral  lesion  has  been  found  atrophied. 

2.  Parencephalus  is  a  name  first  given  by  Heschl  to  the  condition  in 
which  a  loss  of  substance  is  found  in  the  brain,  and  which  is  usually 
filled  with  serous  fluid.  The  cavity  is  generally  situated  on  the  surface 
of  the  cerebral  hemisphere ;  on  one  side  it  may  open  into  the  arach- 
noid sac,  or  be  separated  from  it  by  the  viscei'al  arachnoid,  and  on  the 
other  side  it  may  penetrate  the  whole  extent  of  the  medullary  sub- 
stance so  as  to  reach  the  ependyma  or  to  communicate  freely  with  the 
lateral  ventricle.  The  defect  may  be  only  of  small  extent,  but  it  is 
sometimes  associated  with  hydrocephalus,  and  it  may  then  extend  over 
the  whole  mantle  of  the  hemispheres  as  far  as  the  basal  ganglia,  while 
all   intermediate    sizes  may  be  found  between   these  extremes.     The 


498 


THE    SPASMODIC    PARALYSES. 


cerebral  defect  may  be  acquired  or  congenital.  The  ac(|uired  varieties 
may  occur  at  alf  ages,  and  they  are  chiefly  caused  by  embolism  or 
hemorrhage,  although  they  may  occasionally  result  from  injury.  Tlie 
lesion  may  be  situated  in  any  area  of  the  cerebral  hemisphere,  but  in 
the  majority  of  cases  it  occupies  the  area  of  the  Sylvian  artery,  and  it 
is  then  accompanied  by  descending  degeneration  of  the  corresponding 
pyramidal  tract.  Congenital  parencephalus  may  be  caused  either  by  a 
destructive  lesion  or  by  an  arrest  of  development. 

When  the  cavity  has  been  caused  by  a  destructive  lesion  its  Avails 
are  formed  of  cicatricial  tissue,  and  it  is  probable  that  evidences  of 
sclerosis  of  the  pyramidal  tracts  of  the  cord  will  be  found  on  micro- 
scopical examination,  but  this  point  has  not  been  fully  investigated  in 
the  recorded    cases.     In    the   congenital  variety,  caused  by  arrest  of 

Fig.  150. 


development  of  the  brain,  the  Avails  of  the  cavity  are  formed  by  the 
ependyma  of  the  lateral  ventricles,  and  by  the  gray  matter,  which  to 
the  naked  eye  has  all  the  appearance  of  the  healthy  cortex,  but  showing 
deficiency  of  the  motor  ganglion  cells  on  microscopical  examination. 
In  some  cases  a  defect  in  the  parietal  bone  is  present  immediately  over  the 
defect  in  the  brain.  A  case  of  this  kind  was  examined  at  a  post-mortem 
by  Meschede,  and  I  have  recorded  a  case  of  defect  of  the  parietal  bone 
(Fig.  159)  associated  with  congenital  hemiplegia  of  the  opposite  half 
of  the  body,  and  in  which  a  parencephalous  defect  most  probably  existed 


MORBID    ANATOMY, 


499 


immediately  underlying  the  osseous  defect.  In  parencephalus  from 
arrest  of  development  a  cavity  often  exists  at  symmetrical  points  in 
each  hemisphere,  and  the  antero-lateral  columns  of  the  cord,  instead  of 
being  in  a  state  of  sclerosis,  are  small  in  size  and  defective  in  develop- 
ment, as  in  a  case  recorded  by  myself  (Fig.  160).  When  the  paren- 
cephalous  defect  is  unilateral  the  anterior  colmnn  of  the  cord  on  the 
same  side  and  the  lateral  column  on  the  opposite  side  are  much  less  in 
size  than  the  corresponding  columns  the  fibres  of  which   are  derived 

Fig.  160. 


from  the  healthy  side.  This  fact  was  well  illustrated  in  a  case  of  paren- 
cephalus shown  b}^  Dr.  Shuttleworth,  of  the  Albert  Asylum,  at  a  meet- 
ing of  the  Manchester  Medical  Society.  It  is  very  likely  that  bilateral 
athetosis,  and  other  cases  of  infantile  motor  disorders  associated  with 
idiocy,  are  caused  by  a  parencephalous  defect  of  one  or  both  hemi- 
spheres of  the  brain. 

Very  little  is  known  with  regard  to  the  morbid  anatomy  of  the  spastic 
paraplegias  of  infancy.  In  most  of  these  cases  the  spastic  condition  of 
the  extremities  is  cono-enital,  and  cvenerallv  associated  with  difficulties 
of  articulation  and  other  evidences  of  disordered  cerebral  function,  and 
consequently  it  is  probable  that  the  symptoms  are  caused  by  a  small 
parencephalous  defect  in  each  hemisphere  of  the  brain. 


IV.    MOXOPLEGIA. 

It  has  just  been  seen  that  ordinary  hemiplegia  is  caused  by  destruc- 
tive lesions   in   or  near  the  fibres  of  the  pyramidal  tract,  as  they  lie 


600 


THE    SPASMODIC    PARALYSES. 


near  together  in  the  internal  capsule.  In  the  corona  racliata  these 
fibres  form  more  or  less  separate  bundles  corresponding  to  the  motor 
centres  in  the  cortex,  so  that  destructive  lesions  of  the  centrum  semi- 
ovale  or  of  the  cortex,  provided  the  whole  thickness  is  destroyed,  may 
injure  one  of  these  bundles  whilst  leaving  the  others  intact,  and  conse- 
quently localized  lesions  in  these  positions  give  rise  to  a  monoplegia. 
It  must,  however,  be  remembered  that  extensive  lesions  of  the  cortex 
of  the  motor  area  of  the  brain  will  cause  a  comi)lete  hemiplegia  whicli 
differs  scarcely  in  any  respect  from  the  hemiplegia  which  results  from 
disease  of  the  internal  capsule. 

1.   Crural  Monoplegia. 

A  few  cases  of  disease  of  the  cortex  of  the  brain  are  recorded  in 
which  the  paralysis  was  limited  to  the  leg.  In  a  case  reported  by  Dr. 
Huddon  the  paralysis  was  limited  to  the  left  leg  for  five  months,  but 
after  a  time  the  left  arm  also  became  paralyzed.  After  death  a  tumor 
three  inches  in  diameter  was  found  connected  with  the  dura  mater;  it 

Fi(i.  161. 


was  situated  to  the  right  of  the  middle  line  and  compressed  the  sub- 
jacent hemisphere,  and  destroyed  the  upper  extremities  of  tlie  ascend- 
ing frontal  and  parietal  convolutions  and  the  i)ostero-parietal  lobule 
(Fig.  162)  as  well  as  the  paracentral  lobule  (Fig.  161). 

2.  Brachio-crural  Monoplegia. 

Paralysis  of  the  leg  and  arm  are  frequently  associated  in  disease  of 
the  cortex.  A  case  of  paralysis,  with  rigidity  of  the  leg  and  arm,  of 
three  years'  duration,  is  reported  by  Charcot  and  Pitres,  in  which  a 
patch  of  softening  was  found  at  the  upper  extremity  of  the  fissure  of 
Rolando  on  the  convex  surface  of  the  right  hemisphere.     Pitres  de- 


MORBID    ANATOMY, 


501 


scribes  a  case  of  paralysis  with  unilateral   convulsions  of  the  left  ex- 
tremities, in  which  a  focus  of  softening  was  found  not  in  the  cortex,  but 


Fig.  162. 


Fig.  163. 


in  the  centrum  ovale,  immediately  beneath  the  posterior  extremity  of 
the  first  frontal  convolution  (Fig.  163),  and  extending  backwards  under- 
neath the  superior  parietal  lobule. 


602  THE    SPASMODIC    PAEALYSES. 

3.  Brachial  Monoplegia. 

A  large  number  of  cases  of  brachial  monoplegia  from  cortical  disease 
have  been  collected  and  analyzed  by  Decaisne,  but  it  would  occupy  too 
much  space  to  quote  them  here.  The  lesions  have  been  found  in  the 
ascending  frontal  and  parietal  convolutions. 

4.  Bracliio'facial  Monoplegia. 

Paralysis  of  the  face  and  arm  is  not  infrequently  associated  in  dis- 
ease in  or  near  the  cortex,  and  when  the  left  hemisphere  is  the  seat  of 
lesion  the  paralysis  is  accompanied  by  aphasia.  In  these  cases  the 
lesion  has  been  found  near  the  inferior  part  of  the  fissure  of  Rolando 
on  a  level  with  the  posterior  part  of  the  third  frontal  convolution.     In 

Fig.  164. 


other  cases  the  lesion  is  situated  in  the  white  substance.  A  case,  for 
example,  is  reported  by  Anton  Frey  in  which  the  left  arm  and  the  left 
side  of  the  face  were  paretic,  and  in  which  a  focus  of  softening  was 
found  in  the  white  substance  at  the  junction  of  the  middle  frontal  with 
the  ascending  frontal  convolutions  (Fig.  104). 

5.  Facial  Monoplegia. 

Facial  paralysis  of  cerebral  origin  is  generally  complicated  by  aphasia 
and  paralysis  of  the  arm,  but  a  few  uncomplicated  cases  of  this  form  of 
paralysis  have  been  observed.  Hitzig  relates  the  case  of  a  soldier 
who  had  received  a  bullet  wound  on  the  right  side  of  the  head,  and 
became  aiFected  two  months  subseiiuently  by  clonic  spasm  of  the  left 
side  of  the  fiice,  followed  by  paralysis  of  those  muscles  and  of  the 
left  half  of  the  tongue.  After  death  an  abscess  was  found  correspond- 
ing to  the  seat  of  the  injury  in  the  ascending  frontal  convolution  be- 


MORBID    ANATOMY.  503 


tween   the  paracentral  fissure  and  the  fissure  of  Rolando  (Fig,  165). 
This  case  and  others  show  that  the  lesion  in  facial  monop^.eoia  of  corti- 


FiG.  ^p>' 


cal  origin  is  situated  in  or  near  the  posterior  extremity  of  the  third 
frontal  convolution, 

6,  Labio-glosso-Iari/m/eal  Paralysis  of  Cerebral  Origin. 

The  symptoms  of  a  progressive  labio-glosso-laryngeal  paralysis  are 
sometimes  closely  simulated  by  lesions  of  the  hemispheres  of  the  brain. 
Dr,  Barlow  reports  the  case  of  a  boy,  aged  ten  years,  who  was 
suffering  from  aortic  regurgitation,  and  had  an  attack  of  right  hemi- 
plegia and  aphasia,  from  which  he  made  a  good  recovery.  Four  months 
afterwards  he  had  an  attack  of  left  hemiplegia  with  aphasia,  and  in 
addition  the  muscles  of  mastication  and  articulation  and  those  concerned 
in  the  first  act  of  deglutition,  were  paralyzed.  The  patient  died  of 
the  aortic  disease,  and  at  the  autopsy  evidence  of  an  embolus  was 
found  in  both  Sylvian  arteries,  A  focus  of  softening,  about  the 
size  of  a  shilling,  was  found  in  the  cortex  of  each  hemisphere,  involving 
the  inferior  extremity  of  the  ascending  frontal,  and  the  posterior 
extremities  of  the  second  and  third  frontal  convolutions.  In  a  case 
reported  by  Magnus  and  (pioted  by  Romberg,  not  only  were  the  symp- 
toms of  bulbar  paralysis  ])resent,  but  the  upper  fixcial  muscles  were 
likewise  paralyzed,  and  after  death  only  one  hemorrhagic  cyst,  which 
was  about  the  size  of  a  small  walnut,  was  found,  the  situation  of  this 
cyst  evidently  being  the  centrum  semiovale  of  the  right  hemisphere 
immediately  underlying  the  posterior  part  of  the  third  frontal  convolu- 
tion. Several  cases  of  bulbar  paralysis  of  cerebral  origin  have  now 
been  reported  in  which  the  lesions  were  found  in  the  lenticular  nucleus 
of  both  hemispheres.  Bulbar  paralysis  occurring  in  sclerosis  in  patches 
is  sometimes  caused  by  a  patch  of  sclerosis  in  each  lenticular  nucleus, 


504  THE    SPASMODIC    PARALYSES. 

but  these  symptoms  Avhen  of  cerebral  origin  usually  occur  in  those  who 
are  suffering  from  granular  kidney,  or  from  syphilis  of  the  cerebral 
vessels.  The  general  history  of  such  cases  is  that  the  patient  has  an 
attack  of  right-sided  hemiplegia  with  aphasia,  the  aphasia  rapidly  dis- 
appears and  recovery  takes  place  from  the  hemiplegia  to  such  an  extent 
that  the  paralysis  is  scarcely  perceptible,  but  the  tendon-reactions  are 
slightly  exaggerated.  Some  months  after  the  first  attack  the  patient 
suffers  from  an  attack  of  left-sided  hemiplegia  with  aphasia  ;  the  aphasia 
soon  disappears  after  this  attack  also,  and  the  limbs  recover,  so  that  there 
is  only  a  slight  diminution  of  the  motor  power  remaining,  but  the 
tendon-reactions  remain  exaggerated,  and  noAV  the  patient  is  found  to  be 
suffering  from  all  the  usual  symptoms  of  bulbar  paralysis.  In  these 
cases  the  lenticular  nucleus  in  each  hemisphere  is  found  to  contain  a 
cyst  filled  with  serous  fluid,  the  result  of  hemorrhage  or  of  softening. 
The  symptoms  are,  however,  caused,  probably  not  by  the  disease  of  the 
lenticular  nuclei  themselves,  but  by  partial  damage  of  the  fibres  of  the 
pyramidal  tract  which  pass  on  each  side  through  the  knees  of  the 
internal  capsule  and  which  connect  the  posterior  part  of  the  third  frontal 
convolution  witli  the  bulbar  motor  nuclei. 

7.    Unilateral  Ofulo-niotor  Blonoplcgia. 

It  has  already  been  mentioned  that  conjugate  deviation  of  the  eyes 
and  rotation  of  the  head  and  neck  are  frequent  symptoms  both  of  con- 
vulsions and  hemiplegia,  and  that  the  deviation  in  the  former  is  directed 
away  from  and  in  the  latter  towards  the  hemisphere  in  whicli  the  lesion 
is  situated.  In  the  brain  of  the  monkey  Ferrier  localizes  a  centre  in 
the  posterior  extremity  of  the  second  frontal  convolution,  irritation  of 
Avhich  causes  elevation  of  the  eyelids,  dilatation  of  the  pupils,  conjugate 
deviation  of  the  eyes  and  turning  of  the  head  to  the  opposite  side ;  and 
he  also  found  that  extensive  movements  of  the  eyeballs,  along  with  asso- 
ciated movements  of  the  head  and  neck  result  from  irritation  of  the 
supramarginal  and  angular  gyri.  One  or  two  cases  are  recorded  which 
render  it  probable  tluit  lesion  of  the  posterior  extremity  of  the  second 
frontal  convolution  will  cause  conjugate  deviation  of  the  eyes  and 
rotation  of  the  liead  and  neck  in  man,  but  the  recorded  cases  are  not 
conclusive  upon  this  point.  Numerous  cases,  however,  have  been  re- 
corded in  which  this  symptom  was  caused  by  a  lesion  in  or  near  the 
angular  gyrus.  Grasset  has  collected  much  evidence  upon  this  point 
and  he  has  recorded  a  case  of  his  own  in  which  the  patient  suffered 
from  left-sided  hemiplegia  and  a  conjugate  deviation  of  the  eyeballs 
with  rotation  of  the  head  directed  to  the  right,  and  in  which  the  disease 


MORBID     ANATOMY. 


505 


consisted  of  lesion  of  the  pli  courh  of  the  right  hemisphere  (Fig.  166). 
Many  cases  are  also  reported  in  which  conjugate  deviation  of  the  eyes 
was  caused  by  disease  of  the  centrum  ovale  and  in  these  cases  the  lesion 
was,  as  a  rule,  situated  between  the  internal  capsule  and  the  supra- 


Fio.  166. 


marginal  and  angular  gyri.  It  would  also  appear  that  disease  in  the 
neighborhood  of  the  angular  gyrus  and  supraniarginal  lobule  produces 
at  times  paralysis  of  the  levator  palpebrfe  superioris  of  the  opposite 
side,  without  the  other  muscles  supplied  by  the  third  nerve  being  im- 
plicated. 

8.  Hemiplegia  from  Cortical  Disease. 

A  case  of  complete  hemiplegia  of  the  right  side,  of  six  years'  dura- 
tion is  described  by  Lepine  in  which  there  was  total  destruction,  caused 

Fig.  167. 


by  yellow  softening,  of  the  ascending  parietal  convolution,  and  partial 
destruction  of  the  Island  of  Reil,  ascending  frontal  convolution,  and  the 


506 


THE    SPASMODIC    PARALYSES, 


anterior  part  of  the  superior  and  inferior  parietal  lobules  of  tlie  left 
hemisphere  (Fig.  167).  Secondary  degeneration  was  traced  in  the  left 
half  of  the  pons  and  in  the  pyramid  of  the  medulla.  Several  similar 
cases  are  reported  by  others.  Dussaussay  describes  a  case,  quoted  hj 
Pitres,  of  right  hemiplegia  with  conjugate  deviation  of  the  eyes  to  the 
left,  and  in  which  a  cavity  Avas  found  in  the  centrum  ovale  of  the  left 
hemisphere  containing  dark  coagulated  blood  (Fig.  168).     This  cavity 

Fig.  168. 


was  limited  internally  by  the  gray  substance  of  the  paracentral  lobule ; 
superiorly  and  externally  by  the  gray  substance  of  the  ascending  frontal 
and  parietal  convolutions  :  in  front  it  extended  to  the  pnuceiitral  fissure  : 
and  behind  to  the  posterior  border  of  the  ascending  parietal  convolu- 
tions ;  while  inferiorly  it  was  separated  from  the  corpus  striatum  by  a 
thin  layer  of  white  substance. 

Morbid  Physiology. — In  primary  lateral  sclerosis  conduction  through 
the  fibres  of  the  pyramidal  tracts,  which  convey  voluntary  impulses  from 
the  cortical  motor  centres  to  the  spinal  cord,  is  wholly  or  partially 
arrested,  and  consequently  voluntary  paralysis  results.  The  spinal 
centres  with  the  reflex  arcs  are,  however,  uninterfered  with,  and  as  they 
are  now  set  free  from  the  inhibitory  influence  of  the  cerebrum  the 
reflexes  and  tendon-reactions  become  increased.  Dr.  Hu2hlin<:rs-Jack- 
son  has  suggested  that  the  muscular  tension  and  contractures  are  caused 
by  the  unantagonized  influence  of  the  cerebellum  on  the  paralyzed 
muscles,  but  this  theory  is  not  free  from  difficulty. 

Amyotrophic  lateral  sclerosis  is  caused,  according  to  Charcot,  by  a 
primary  lateral  sclerosis  to  which  disease  of  the  anterior  gray  horns 


MORBID    ANATOMY.  507 

becomes  superadded,  the  lesion  beginning  in  the  cervical  region  and  sub- 
sequently extending  upwards  to  the  medulla  oblongata  and  downwards 
to  the  lumbar  region.  The  presence  of  lateral  sclerosis  explains  the 
facts  that  the  paralysis  often  precedes  the  atrophy,  and  is  associated  with 
muscular  tension,  contractures,  and  exaggerated  tendon-reactions  ;  Avhile 
the  presence  of  disease  of  the  ganglion  cells  explains  the  muscular 
atrophy  which  becomes  associated  with  the  paralysis.  But  the  paralysis 
of  the  upper  extremities  is  sometimes  of  the  pure  atrophic  variety,  and 
I  cannot  help  thinking  that  in  some  cases  at  least  the  lesion  begins  in 
the  gray  matter  and  extends  outwards  to  the  lateral  columns. 

In  disease  of  the  substance  of  the  cerebral  hemispheres  and  of  the 
basal  ganglia,  hemiplegia  is  caused  by  arrest  of  conduction  through  the 
fibres  of  the  pyramidal  tract.  If  the  clot  simply  compresses  these 
fibres  without  rupturing  them,  recovery  takes  place  when  the  eflPused 
blood  is  absorbed,  but  if  these  fibres  are  ruptured  the  hemiplegia 
becomes  permanent.  It  is  very  probable  that  early  rigidity  occurring 
at  the  time  of  the  hemorrhage  is  caused  by  rupture  of  these  fibres, 
while  the  rigidity  which  begins  a  few  days  after  the  attack  is  caused 
by  an  inflammation  of  the  fibres  excited  by  the  presence  of  the  clot, 
which  acts  as  a  foreign  body.  Late  rigidity  comes  (in  about  the  same 
time  as  the  descending  changes  in  the  pyramidal  tract,  and  is  produced 
by  the  same  mechanism  as  the  spastic  rigidity  of  the  limbs  in  primary 
spinal  lateral  sclerosis.  It  is  not  easy  to  give  reasons  why  choreiform 
movements  are  so  liable  to  occur  wdien  the  lesion  is  situated  in  the  area 
of  the  posterior  external  optic  artery.  Two  probable  explanations  of 
these  clonic  spasms  suggest  themselves  to  my  mind.  The  first  is  that 
fibres  connecting  the  cerebrum  with  the  cerebellum  are  injured  by  these 
lesions,  so  that  the  normal  proportion  between  the  outgoing  discharges 
which  regulate  the  tonic  (cerebellar)  and  the  clonic  (cerebral)  actions  of 
the  body  is  lost.  The  second  is  that  the  spasms  are  caused  by  partial 
injury  of  the  fibres  of  the  pyramidal  tract  which  regulate  the  funda- 
mental actions.  The  fundamental  actions  are  regulated  from  the  con- 
volutions near  the  longitudinal  fissure,  and  the  special  actions  from  the 
convolutions  which  border  the  Sylvian  fissure,  :ind  it  is  manifest  that 
the  fibres  which  descend  in  the  corona  radiata  from  the  former  will  pass 
on  the  optic  thalamus  side  of  the  internal  capsule,  while  those  which 
descend  from  the  latter  Avill  pass  on  the  lenticular  nucleus  side  of  it. 
Injury  of  the  optic  thalamus  will,  therefore,  be  likely  to  damage  the 
fundamental  fibres  of  the  pyramidal  tract,  while  leaving  the  accessory 
fibres  unaff'ected.  The  eifect  of  impairment  of  the  fundamental  actions 
might  well  be  to  cause  the  voluntary  and  special  actions  to  be  effected 
with  irregularity  and  want  of  harmony.     The  only  interpretation  which 


508  THE    SPASMODIC    PARALYSES. 

the  spastic  paralyses  of  infancy  admit  of,  is  that  the  cerebral  motor 
mechanism  in  one  or  both  hemispheres  is  either  destroyed  by  a  lesion 
after  its  development,  or  that  the  development  of  the  motor  mechanism 
is  defective  from  the  first  or  completely  arrested. 

The  morbid  physiology  of  the  functional  paralyses  is  somewhat  obscure. 
Post-epileptic  paralysis  is  most  probably  induced  by  the  exhaustion  of 
the  motor  cortical  centres  caused  by  a  previous  excessive  discharge,  just 
as  the  sciatic  nerve  of  a  frog  is  paralyzed  for  a  time  by  passing  a  strong 
faradic  current  through  it.  Hysterical  paralysis  is  also  best  explained 
by  supposing  that  the  molecules  of  the  cells  of  the  motor  centres  of 
the  cortex  are  in  a  state  of  stable  equilil)rium,  and  consequently  im- 
pulses from  the  cortex  fail  to  be  conducted  outwards  to  the  muscles 
through  the  fibres  of  the  pyramidal  tract.  It  is  still  more  difficult  to 
give  an  explanation  of  the  toxic  paralyses.  It  is  impossible  for  us  to 
tell  why  curara  acts  on  the  intramuscular  nerve  endings,  atropine  on 
the  vagi,  and  lead  on  certain  peripheral  nerves ;  we  must  accept  the 
facts  as  they  are  disclosed  by  experiment  and  observation  and  generalize 
them  as  best  we  can. 

Treatment. — The  treatment  of  the  spasmodic  paralyses  will  depend 
upon  the  primary  lesion  which  causes  the  sclerosis  of  the  lateral  columns 
which  underlies  the  paralysis.  Primary  sclerosis  of  the  lateral  columns 
of  the  cord  must  be  treated  internally  like  other  cases  of  chronic 
myelitis  by  iodide  of  potassium,  while  the  galvanic  current  is  the  most 
trustworthy  local  remedy.  A  carefully  conducted  hydropathic  treat- 
ment may  sometimes  be  beneficial,  and  gaseous  thermal  springs  have 
been  employed  with  advantage.  Local  stimulating  treatment  by  means 
of  the  faradic  current  and  massage  must  be  avoided  in  all  forms  of 
spasmodic  paralysis.  Amyotrophic  lateral  sclerosis  must  be  treated  on 
the  same  general  principles  as  other  forms  of  chronic  myelitis.  In 
secondary  sclerosis  of  the  lateral  columns  of  the  cord  the  case  must  be 
carefully  investigated  with  a  view  to  discover  whether  the  primary  lesion 
is  situated  in  the  vertebrae,  membranes,  or  cord  itself,  and  then  the 
nature  of  the  lesion,  whether  inflammatory,  scrofulous,  or  syphilitic, 
should  be  determined,  and  the  treatment  must  be  conducted  accordino-lv. 
In  hemiplegia  and  monoplegia  the  locality  of  the  lesion  must  first  be 
investigated  and  then  an  endeavor  must  be  made  to  determine  whether 
the  lesion  is  likely  to  be  a  hemorrhage,  embolism,  thrombosis,  or  a 
tumor.  The  treatment  of  these  morbid  conditions  Avill  be  subsequently 
described.  The  local  treatment  of  the  paralyzed  limbs  consists  of  the 
application  of  the  galvanic  current,  and  a  moderate  degree  of  rubbing 
of  the  surface,  but  deep  kneading  of  the  muscles,  and  the  application 
of  the  faradic  current  or  any  other  stimulating  measures,  must  be  avoided. 


CHAPTER     IX. 

DISORDERS  OF  MOTOR  COORDINATION. 

1.  MENIERE'S  DISEASE  (AURAL  OR  LABYRINTHINE  VERTIGO). 

Etioloiji). — Aural  vertigo,  as  described  by  Meniere,  comes  on  suddenly 
and  Avithout  apparent  cause.  Acute  and  chronic  catarrh  of  the  middle 
ear  and  inflammation  of  the  labyrinth  are  often  accompanied  by  deaf- 
ness and  severe  vertigo,  and  transient  vertigo  may  be  caused  by  the 
impulsion  of  air  or  fluids  through  the  Eustachian  tube  into  the  tym- 
panic cavity,  by  external  pressure  on  the  drum-head,  by  wax  or  other 
accumulation  in  the  meatus,  or  by  the  passage  of  a  galvanic  current 
through  the  ears.  Aural  vertigo  with  deafness  is  sometimes  one  of 
the  earliest  symptoms  of  locomotor  ataxia. 

Symptoms. — The  characteristic  symptoms  of  Meniere's  disease  are 
sometimes  preceded  by  partial  deafness,  earache,  and  other  indications  of 
a  local  disease,  but  in  other  cases  the  patient  is  suddenly  attacked  with 
deafness,  noises  in  the  ears,  and  a  feeling  of  giddiness,  Avhich  is  attended 
by  fainting,  nausea  and  vomiting.  The  attack  passes  off  in  a  few 
seconds  or  minutes,  but  recurs  after  a  variable  period,  the  paroxysms 
becoming  more  aggravated,  and  more  frequently  repeated  as  the  dis- 
ease advances.  The  noise  is  sometimes  heard  in  both  ears,  but  is 
probably  always  more  pronounced  on  one  side  than  the  other ;  it  is 
compared  to  the  loud  whistling  of  a  steam  engine  or  to  a  succession  of 
explosions,  or  is  described  as  a  continuous  humming  or  buzzing.  The 
noise  ceases  with  the  attack  in  recent  or  slight  cases,  but  continues  to 
distress  the  patient  during  the  interval  in  long-standing  and  severe 
cases. 

The  attack  of  vertigo  varies  in  duration  and  intensity.  In  slight 
cases  it  consists  of  a  momentary  feeling  of  swimming  in  the  head,  but 
in  severe  cases  each  paroxysm  may  extend  over  a  period  of  ten  or  more 
minutes,  Avhile  in  still  more  aggravated  cases  tlie  feeling  of  uncertainty 
and  giddiness  is  never  absent  during  waking  hours,  and  every  effort  on 
the  part  of  the  patient  to  assume  the  erect  posture  determines  a  parox- 
ysm of  vertigo,  nausea,  and  vomiting.  During  the  paroxysm  the 
patient  feels  as  if  he  were  rotating  round  a  vertical  or  liorizontal  axis, 
or  as  if  he  were  falling  forwards,  backwards,  or  laterally :  he  staggers 


510  DISORDERS    OF    MOTOR    CO  -  0  RDIX  ATIOX  . 

and  clutches  at  surrounding  objects,  or  actually  flills  in  the  direction  in 
which  his  abnormal  sensations  would  lead  him  to  expect.  The  patient 
also  feels  faint,  and  occasionally  actual  syncope  may  occur;  the  skin 
then  becomes  pallid,  cold,  and  covered  with  sweat,  pulse  is  feeble  and 
flickering,  the  patient  suffers  from  confusion  of  ideas,  and  in  aggravated 
cases  there  may  be  a  transitory  loss  of  consciousness,  and  there  is  an 
intense  feeling  of  nausea  Avhich  often  terminates  in  vomiting,  when  the 
attack  usually  comes  to  an  end.  Oscillatory  movements  of  the  eyeballs 
have  in  some  cases  been  observed  during  the  attack,  and  in  these  cases 
there  was  an  apparent  displacement  of  objects  with  reference  to  the 
patient.  When  one  ear  is  exclusively  aff"ected  w^ith  noises  and  deafness 
the  i)atient  may  experience  a  constant  tendency  to  walk  to  the  opposite 
side.  It  was  shown  by  Hinton  that  perception  of  musical  notes  is  often 
faulty  in  this  disease;  in  one  case  observed  by  him  G-  of  the  third 
octave  was  heard  as  C  of  the  octave  below,  or  twelve  notes  below  the 
normal  pitch,  and  more  or  less  similar  results  were  obtained  with  other 
notes. 

The  course  of  the  disease  is  a  steadily  progressive  one  until  complete 
deafness  is  established,  when,  fortunately,  all  the  distressing  symptoms 
of  the  disease  cease.  The  paroxysms  of  vertigo  come  on  at  first  at 
irregular  intervals;  they  increase  gradually  in  frequency  and  intensity, 
and  in  aggravated  cases  the  patient  suffers  continuously  from  some 
degree  of  vertigo,  while  he  is  liable  to  paroxysmal  exacerbations  of 
great  severity.  The  noises  in  the  ears  may  cease  at  first  during  the 
intervals,  but  after  a  time  they  are  constant  during  waking  hours  until 
the  patient  is  completely  deaf. 


2.  PRI3IARY  SCLEROSIS  OF  THE  COLUMNS  OF  GOLL. 

Only  a  few  cases  which  can  ho  regarded  as  a  primary  affection  of 
the  columns  of  Goll  are  recorded.  In  a  case  recorded  by  I'ierret  the 
symptoms  consisted  of  a  girdle  sensation  passing  round  the  body,  light- 
ning pains  and  various  other  sensory  disorders  in  the  lower  extremities, 
and  inability  to  maintain  the  erect  posture  with  closed  eyes,  while  on 
wishing  to  advance  the  patient  felt  as  if  she  were  drawn  backwards,  but 
once  started  she  was  impelled  forwards  by  an  uncontrollable  force.  The 
patient  died  at  the  age  of  thirty  years  from  an  attack  of  acute  pneu- 
monia, and  at  the  autopsy  Pierret  discovered  the  presence  of  sclerosis 
of  the  columns  of  Goll.  The  posterior  root-zones  were,  however,  im- 
plicated in  the  lesion  to  some  slight  extent  in  the  dorsal  region,  and, 
judging  from  the  drawings  which  accompany  the  report  of  the  case,  in 


PEOGRESSIVE    LOCOMOTOR    ATAXIA.  oil 

tlie  lumliar  region  also.  The  case  cannot,  therefore,  be  regarded  as  a 
typical  example  of  sclerosis  of  the  columns  of  Goll.  A  case  of  primary 
sclerosis  of  the  columns  of  Goll  has  been  reported  by  DuCastel  and 
another  by  Gowers,  but  in  neither  were  there  symptoms  durino-  life 
Avhich  could  -with  probability  be  attributed  to  disease  of  these  columns. 


3.  SECONDAKY  SCLEROSIS  OF  THE  COLUMIS'S  OF  GOLL  AKD  OF 
THE  DIRECT  CEREBELLAR  TRACTS. 

These  affections  are  only  of  anatomical  interest  inasmuch  as  they  do 
not  give  rise  to  any  recognizable  symtoms. 


4.  PROGRESSIVE  LOCOMOTOR  ATAXIA  (TABES  DORSALIS,  GRAY 
DEGENERATION  OR  SCLEROSIS  OF  THE  POSTERIOR  COLUMNS 
OF  THE  SPINAL  CORD). 

Etiology. — Locomotor  ataxia  often  occurs  in  individuals  whose  nearest 
relatives  have  suffered  from  other  nervous  diseases,  such  as  monomania, 
hypochondriasis,  epilepsy,  migraine,  mental  disease,  or  violent  fits  of 
anger  and  drunkenness.  In  other  cases  the  heredity  is  direct  from 
parent  to  offspring.  Friedreich  met  with  three  different  ftimilies  in 
which  several  brothers  and  sisters  were  attacked  with  the  disease  about 
the  same  age,  while  the  parents  themselves  were  healthy,  and  Carre 
was  informed  by  an  ataxic  patient  that  eighteen  other  members  of  her 
family  were  affected  by  the  same  disease.  Locomotor  ataxia,  according 
to  the  statistics  of  Eulenburg,  attacks  males  in  the  proportion  of  one 
hundred  and  twenty-eight  to  twenty-one  females.  It  is  essentially  a 
disease  of  youtli  and  middle  age,  by  fiir  the  larger  number  of  cases 
occurring  between  the  ages  of  twenty  and  fifty  years,  although  it  has 
been  observed  occasionally  in  children. 

The  exciting  causes  of  locomotor  ataxia  are  exposure  to  cold  and 
damp,  severe  bodily  and  mental  exertion,  emotional  disturbances,  sexual 
excesses,  and  injuries  of  various  kinds,  such  as  a  fracture  of  the  thigh 
or  concussion  of  the  spinal  cord.  It  is  sometimes  the  sequel  of  acute 
disease,  such  as  typhus,  articular  rheumatism,  acute  pneumonia,  and 
diphtheria,  and  of  repeated  abortions  and  the  puerperal  state. 

But  of  all  the  antecedents  of  locomotor  ataxia,  syphilis  is  the  most 
frequent  and  most  important  factor  in  its  genesis.  Fournier  stated,  in 
1876,  that  syphilis  had  preceded  locomotor  ataxia  in  twenty-four  out  of 
thirty  cases  observed  by  him.   and  soon  afterwards  "N^ilpian  asserted 


512  DISOEDEES    OF    MOTOE    CO  -  OEDIN  ATIOX. 

that  about  seventy-five  per  cent,  of  patients  suffering  from  locomotor 
ataxia  are  old  syphilitic  subjects.  In  the  more  recent  statistics  of  Erb, 
Fournier,  and  others,  the  frequency  with  which  ataxia  attacks  syphilitic 
subjects  is  placed  as  high  as  from  eighty-nine  to  ninety-one  per  cent,  of 
all  cases,  while  Fischer,  Westphal,  and  others  do  not  find  the  propor- 
tion higher  than  from  fourteen  to  twenty  per  cent.  My  own  experience 
agrees  with  the  higher  rather  than  the  lower  percentages.  Locomotor 
ataxia  is  one  of  the  tertiary  manifestations  of  syphilis,  but  Fournier 
met  with  a  case  in  which  the  symptoms  of  tabes  began  twenty-tA\o 
months  after  the  primary  infection,  and  during  the  secondary  symptoms; 
in  other  cases  an  interval  of  upwards  of  twenty  years  elapsed  between 
the  infection  and  the  first  ap})earance  of  the  tabetic  symptoms,  but  the 
majority  of  cases  of  syphilitic  ataxia  occur  between  the  sixth  and  twelfth 
years  after  infection.  It  is  important  to  notice  that  locomotor  ataxia 
succeeds  with  much  greater  frequency  to  the  milder  than  to  the  severer 
forms  of  syphilitic  infection,  and  Fournier  has  shown  that  an  efficient 
mercurial  treatment  during  the  early  period  of  syphilis  greatly  dimin- 
ishes the  liability  to  ataxia. 

Symptoms. — The  course  of  locomotor  ataxia  may,  for  the  i)urposes 
of  description,  be  divided  into  three  stages :  (1)  The  premonitory  or 
preataxic  stage  ;  (2)  the  ataxic  stage ;  and  (3)  the  paralytic  stage,  or 
the  period  of  the  generalization  of  the  ataxia. 


(1)  The  Pkkataxic  Stage. 

The  symptoms  of  tlie  preataxic  stage  may  be  subdivided  into  dis- 
orders of  (a)  general  sensibility  ;  {b)  the  general  motor  functions  apart 
from  ataxia ;  {c)  the  special  senses ;  (d)  the  cranial  motor  and  mixed 
nerves  with  the  cilio-sj)inal  region  of  the  cord :  (/)  the  nutritive  func- 
tions ;  and  (//)  the  cerebral  and  psychical  functions. 

(a)  Disorders  of  G-eneral  Sensibility. — The  most  constant  of  the 
premonitory  symj)toms  of  locomotor  ataxia  -ayc  pains  of  a  peculiar  and 
often  distressing  kind,  which  may  precede  l)y  many  years  all  other 
symptoms,  and  generally  last  throughout  the  whole  course  of  the  disease. 
These  pains  are  compared  by  the  patient  to  forked  lightning  darting 
through  the  body,  and  are  consequently  named  lightning-like  or  lancinat- 
ing pains.  The  lightning  pains  are,  as  a  rule,  not  very  urgent  at  first 
and  are  believed  b}'^  the  patient  to  be  of  rheumatic  origin.  They  con- 
sist of  a  single  dart  which  shoots  suddenly  into  some  j)art  of  the  lower 
extremities,  or  occasionally  of  the  back  of  the  head  or  side  of  the  face, 
and  disappears  as  suddenly  as  it  came,  but  only  to  return  at  no  distant 


PROGRESSIVE    LOCOMOTOR    ATAXIA.  513 

date.  As  the  disease  advances  the  shooting  pains  recur  at  shorter 
intervals,  and  after  a  time  a  number  of  tliem  follow  each  other  so  quickly 
as  to  constitute  a  paroxysm  of  almost  continuous  pain.  The  paroxvsm 
may  last  only  a  few  minutes  at  first,  but  by  and  bye  its  duration  is  pro- 
longed to  some  hours  or  even  days,  during  which  the  patient  suffers  the 
most  excruciating  agony.  The  duration  of  the  interval  between  the 
paroxysms  is  also  very  variable ;  in  some  cases  the  paroxysm  recurs 
every  few  weeks,  but  in  the  interval  the  patient  is  comparatively  free 
from  pain,  Avhile  in  other  cases  the  patients  never  know  what  it  is  to 
have  a  perfectly  free  interval  from  pain,  and  they  are  liable  to  suffer 
every  few  weeks  from  exacerbations  of  great  severity.  The  character 
of  the  pain  also  varies  ;  it  is  sometimes  described  as  burning,  gnawino-,  or 
dragging,  and  during  the  paroxysm  the  pain  is  said  to  shoot  like  light- 
ning through  the  limbs,  or  to  be  like  that  which  would  be  caused  by  a 
sharp  knife  or  red-hot  iron  passing  quickly  through  the  tissues.  The 
lancinating  pains  are  usually  deep-seated  in  the  soft  tissues  or  in  the 
bones,  but  in  addition  to  these,  true  neuralgic  pains,  which  are  limited 
to  the  area  of  distribution  of  a  particular  nerve,  may  supervene  in  the 
course  of  the  disease.  These  neuralgic  pains  sometimes  shift  from  one 
nerve  territory  to  another,  and  do  not  invade  the  same  region  during 
successive  paroxysms  of  pain,  but  at  other  times  the  pain  becomes 
localized  for  a  long  time  in  a  particular  nerve  like  the  sciatic,  and  obsti- 
nately resists  all  treatment. 

Pain  along  the  vertebral  column,  Avhich  is  generally  situated  in  the 
loins  or  between  the  shoulders,  is  another  symptom  of  tabes.  This  pain 
is  dull,  aching,  and  more  or  less  continuous,  but  presents  alternating 
periods  of  remission  and  exacerbation,  and  it  is  only  on  rare  occasions 
that  it  rises  to  any  great  intensity,  and  then  it  may  be  suspected  that 
the  disease  is  complicated  by  a  spinal  meningitis. 

The  girdle  pain  which  is  so  frequently  met  with  in  many  spinal  affec- 
tions is  an  almost  constant  symptom  of  locomotor  ataxia,  and  the  patient 
feels  as  if  a  rope  were  drawn  tight  around  his  body,  or  as  if  it  were 
encircled  by  an  unyielding  iron  ring.  This  sensation  is  usually  situated 
on  a  level  with  the  lower  thoracic  or  upper  abdominal  region,  although 
it  may  occasionally  be  felt  at  the  lower  part  of  the  body  and  it  may 
then  reach  to  the  neck  of  the  bladder.  A  pain  of  similar  character 
may  likewise  be  felt  around  the  joints  of  the  lower  extremities,  and 
patients  then  describe  it  as  a  feeling  like  that  caused  by  a  garter  tied 
tightly  below  the  knee. 

Cutaneous  hypemesthesia  is  not  an  uncommon  symptom  of  the  early 
stage  of  tabes,  and  it  may  be  present  in  several  forms.  At  times  there 
may  be  hypersesthesia  to  impressions  of  temperature  and  anaesthesia  to 

33 


514  DISORDERS    OF    MOTOR    CO  -  ORDIX  ATION. 

touch,  while  at  other  times  anaesthesia  to  touch  may  be  accompanied  by 
a  high  degree  of  hypertesthesia  to  impressions  of  pain.  The  hyper- 
ffisthetic  condition  is  distributed  in  patches,  which  are  often  found  on 
the  lower  extremities  of  patients  suffering  from  severe  paroxysms  of 
lancinating  pains.  Circumscribed  areas  of  skin  then  feel  exquisitively 
sensitive  to  the  slightest  contact,  such  as  a  light  touch  or  the  rubbing 
of  the  clothes,  and  a  slight  touch  on  one  of  these  spots  appears  to  be 
capable  of  determining  an  attack  of  the  lancinating  pains.  These 
hyperresthetic  areas  are  also  subject  to  attacks  of  spontaneous  pain, 
which  is  generally  of  a  scalding  or  burning  character ;  a  patient  once 
compared  this  pain  to  that  Avhich  might  be  caused  by  rubbing  into  the 
skin  a  burning  vesuvian  match. 

Various  paraesthesiae  are  also  experienced  in  the  preataxic  stage  of  the 
disease.  The  patient  suffers  from  the  sensation  popularly  known  as 
"  the  fidgets  "  ;  in  other  cases,  from  a  feeling  of  heat  which  may  be  so 
intense  as  to  compel  him  to  uncover  his  feet  at  night ;  and  in  still 
other  cases  he  is  troubled  with  cold  feet  from  vaso-motor  spasm.  The 
patient  often  complains  of  numbness  and  tingling  of  the  extremities, 
the  soles  of  the  feet  being,  as  a  rule,  the  parts  first  attacked.  Patients 
feel  as  if  they  were  Avalking  on  wool,  cork,  or  felt  soles,  or  upon  bladders 
of  water,  and  in  aggravated  eases  they  have  a  sensation  as  if  the  ground 
were  passing  from  under  their  feet,  or  as  if  they  were  walking  on  air. 
When  their  hands  are  affected  they  feel  as  if  their  fingers  were  covered 
with  gloves,  and  are  then  unable  to  discriminate  the  primary  qualities 
of  objects  which  they  grasp. 

(b)  Disorders  of  the  General  Motor  Functions  apart  from  Ataxia. 
— The  patellar  tendon-reactions  are  usually  absent  at  a  very  early  period 
of  the  premonitory  stage  of  locomotor  ataxia,  and  whenever  these  re- 
actions are  wanting  in  a  person  who  has  for  some  time  been  suffering 
from  recurring  lancinating  pains,  and  who  is  not  the  subject  of  an 
atrophic  paralysis  of  the  quadriceps  femoris  muscle  or  of  diabetes,  there 
is  a  very  strong  presumption  that  he  has  already  entered  upon  the  first 
stage  of  this  progressive  disease.  It  is  possible  that  these  reactions  may 
be  absent  in  a  fcAV  persons  who  are  otherwise  healthy,  while,  on  the 
other  hand,  they  may  be  present  or  exaggerated  in  a  very  few  cases,  in 
which  other  symptoms  strongly  point  to  locomotor  ataxia ;  but  with 
these  slight  reservations  absence  of  the  patellar  tendon-reaction  is  one  of 
the  most  certain  and  valuable  signs  of  the  early  stage  of  locomotor  ataxia. 
The  cutaneous  reflexes  are  usually  unaffected  in  the  early  stage  of 
locomotor  ataxia,  but  as  the  disease  advances  the  normal  interval  between 
the  cutaneous  excitation  and  the  resulting  contraction  may  become 
greatly  prolonged.     In  a  few  cases  the  cutaneous  reflexes  are  greatly 


PROGRESSIVE    LOCOMOTOR    ATAXIA.  515 

exaggerated  even  at  an  advanced  period  of  the  disease.  Paradoxical 
contraction  has  been  observed  by  Westphal  as  a  symptom  of  tabes,  and 
its  presence  may  possibly  be  taken  as  a  sign  that  the  lesion  of  the  pos- 
terior columns  is  extending  to  the  lateral  columns,  and  that  the  paralytic 
stage  of  the  disease  is  approaching. 

Transitory  paresis  of  some  muscular  groups  is  an  occasional  symp- 
tom of  the  early  stage  of  tabes  ;  whilst  walking,  the  legs  may  suddenly 
give  way  at  the  knees  so  that  the  patient  falls  to  the  ground.  This 
sudden  failure  of  motor  power  appears  to  be  comparable  to  the  transitory 
diplopia  which  is  so  common  a  symptom  of  the  preataxic  stage.  In 
other  cases  the  disease  is  ushered  in  by  the  occurrence  of  a  sudden 
paraplegia,  and  it  is  only  after  the  patient  has  recovered  from  the 
paralytic  symptoms  that  the  motor  incoordination  becomes  apparent. 
It  is  probable  that  in  these  cases  the  primary  lesion  had  extended  trans- 
versely so  as  to  have  affected  the  lateral  columns,  and  that  under  treat- 
ment it  has  receded  so  as  to  become  limited  again  to  the  posterior  columns. 
Uncertainty  of  gait  and  station  when  the  eyes  are  closed,  or  when  in 
the  dark,  is  a  motor  symptom  frequently  observed  before  true  ataxia  is 
established.  This  is,  indeed,  frequently  the  first  symptom  to  attract  the 
patient's  attention.  When  he  puts  his  hands  over  his  face  whilst  wash- 
ing, in  the  morning,  he  may  feel  as  though  he  were  swaying  from  side 
to  side,  or  he  may  totter,  and  he  may  be  compelled  to  steady  himself  by 
propping  his  knees  against  the  washstand,  while  his  uncertainty  of  gait 
becomes  very  troublesome  when  he  ascends  a  flight  of  stairs  in  the 
dark,  or  enters  an  unlighted  chamber.  On  careful  observation  of 
the  patient  it  may  be  noticed  that  he  has  a  slight  tendency  to  stagger 
when  he  rises  suddenly  after  sitting  for  some  time,  or  when  he  is  asked 
to  turn  suddenly  round  or  to  walk  backwards,  but  so  long  as  he  walks 
straight  forwards  with  open  eyes  and  in  daylight  there  is  no  staggering 
nor  uncertainty  of  gait.  The  patient  is  also  troubled  at  this  period 
with  attacks  of  vertigo,  which  is  the  subjective  correlative  either  of 
diplopia  or  of  the  uncertainty  of  gait.  Vertigo  is  a  prominent  symptom 
of  the  cases  of  congenital  ataxia  described  by  Friedreich. 

(c)  Affections  of  the  Special  Senses. — Amaurosis  is  a  frequent  and 
distressing  symptom  of  locomotor  ataxia.  Interference  with  sight  is  in- 
dicated by  a  slowly  or  rapidly  advancing  diminution  in  the  acuteness  of 
vision,  and  by  a  restriction  of  the  field  of  vision,  first,  for  the  perception 
of  colors,  and  finally  for  the  recognition  of  objects ;  the  patient  may 
become  blind  at  the  end  of  a  few  weeks,  or  years  may  elapse  before  the 
loss  of  sight  is  complete,  and  occasionally  the  affection  ceases  to  pro- 
gress after  it  has  lasted  for  a  comparatively  long  time.     The  blindness 


516  DISORDERS    OF    MOTOR    CO-ORDINATION. 

is  caused  by  white  atrophy  of  the  optic  disks,  which  is  said  to  appear 
in  about  thirty  per  cent,  of  all  cases  of  tabes. 

Hemiopia  has  been  met  as  a  transitory  symptom  of  the  preataxic 
stage,  but  its  occurrence  is  rare.  Deafness  is  not  an  infrequent  accom- 
paniment of  locomotor  ataxia,  but  it  is  only  in  a  certain  number  of 
these  cases  that  the  loss  of  hearing  can  be  regarded  as  forming  a  part 
of  the  disease,  and  in  such  cases  the  deafness  is  probably  caused  by  a 
parenchymatous  atrophy  of  the  auditory  nerve  analogous  to  that  of 
the  optic  nerve.  Deafness,  with  vertigo  and  the  other  symptoms  of 
Meniere's  disease,  has  occasionally  been  observed  in  the  early  stage 
of  tabes. 

The  olfactory  sense  is  also  occasionally  lost,  a  case  being  described 
by  Althaus  in  which  the  patient  complained  at  first  of  a  subjective 
smell  of  phosphorus,  and  ultimately  lost  all  sense  of  smell. 

The  gustatory  sense  has  not,  so  far  as  I  know,  been  found  aifected, 
although  slight  disturbances  of  the  sense  of  taste  may  be  present  when 
the  trigeminus  is  implicated. 

[d)  Disorders  of  the  Cranial  Motor  and  Mixed  Nerves,  and  of  the 
Cilio-spinal  Region  of  the  Cord.  Paralysis  of  the  Ocular  Muscles. — 
The  symptoms  of  locomotor  ataxia  are  fre(iuently  ushered  in  by  paral- 
ysis of  one  or  more  of  the  ocular  muscles,  the  paralysis  ])eing  at  first 
generally  transient.  After  a  longer  or  shorter  time,  however,  the 
paralysis  recurs  and  becomes  permanent  toAvards  the  later  stages  of  the 
disease.  The  transient  paralyses  of  the  first  stage  are  generally  so  slight 
that  they  declare  themselves  not  by  the  presence  of  a  perceptible  squint, 
but  by  the  sudden  appearance  of  diplopia,  which  is  either  constantly 
present  or  only  when  the  eyes  are  turned  in  particular  directions. 
Distinct  squint  and  ptosis  are,  however,  occasionally  present  in  the 
early  stage,  and  very  frequently  in  the  later  stages  of  the  disease. 
Out  of  sixty-four  cases  of  tabes  collected  by  Eulenburg  twenty-five 
had  strabismus  ;  of  these  twenty-five  cases  nineteen  had  divergent 
strabismus,  and  four  had  in  addition  paralytic  ptosis,  while  six  had 
convergent  strabismus. 

Disorders  of  the  pupils  are  frequently  present  in  a  very  early  stage  of 
locomotor  ataxia.  Of  the  sixty-four  cases  collected  by  Eulenburg  nine 
had  mydriasis,  the  dilatation  being  double  in  three,  single  in  four,  and 
accompanied  by  myosis  of  the  other  in  two  cases,  while  twenty-eight  had 
myosis,  the  contraction  being  double  in  twenty-one  and  single  in  seven 
cases.  Inequality  of  the  pupils  is  common  in  the  early  stage  of  the 
disease,  and  on  the  side  on  which  the  contraction  of  the  pupil  is  the 
more  marked  there  may  be  redness  of  the  cheek,  congestion  of  the 
conjunctiva,  local  elevation  of  temperature,  and  relative  diminution  of 


PROGRESSIVE    LOCOMOTOR    ATAXIA.  517 

the  palpebral  aperture,  while  in  a  few  cases  unilateral  hyperidrosis  of 
the  side  of  the  face  has  been  observed. 

The  Argyll-RoherUon  pupil  is  frequently  present  in  the  early  stage 
of  locomotor  ataxia,  and  it  is  generally,  although  not  invariably  associ- 
ated with  myosis. 

Nystagmus  is  a  very  rare  symptom  of  locomotor  ataxia,  and  is  prob- 
ably never  present  except  in  the  hereditary  form  of  Friedreich. 

The  trigemmus  is  not  unfrequently  implicated  in  tabes.  The  most 
prominent  symptoms  in  the  area  of  distribution  of  this  nerve  are  pains, 
which  may  either  be  neuralgiform  in  character  or  of  the  same  kind  as 
the  lancinating  pains  of  the  lower  extremities.  Both  kinds  of  pain 
may  be  felt  in  the  forehead,  face,  parietal  region,  external  auditory 
meatus,  and  the  lancinating  pains  are  particularly  liable  to  be  felt  in 
and  around  the  orbit.  Paroxysms  of  these  pains  may  sometimes  be 
mistaken  for  hemicrania,  more  especially  as  the  attack  is  often  accom- 
panied by  redness  of  the  conjunctiva,  photophobia,  and  an  increased 
flow  of  tears.  The  attacks  are  usually  followed  by  cutaneous  hyperaes- 
thesia,  but  as  the  disease  advances  the  increased  sensibility  gives  place 
to  anaesthesia  which  is  said  to  occupy  most  frequently  the  conjunctivae 
and  the  nasal  fossae,  but  may  implicate  the  mucous  membrane  of  the 
mouth,  tongue,  and  pharynx  on  one  or  both  sides. 

The  motor  branch  of  the  trigeminus  is  not  so  frequently  affected  as 
the  sensory  branches,  but  occasionally  cases  have  been  observed  in  which 
the  masticatory  muscles  were  the  subjects  of  ataxia,  or  were  so  feeble 
that  the  patient  was  obliged  to  live  upon  pulpy  food. 

1^\\Q  facial  nerve  is  also  occasionally  implicated  in  the  disease,  and 
then  the  face  may  be  contorted  by  grimaces  when  the  patient  speaks, 
from  ataxia  of  the  facial  muscles.  The  muscles  of  the  face,  tongue, 
and  larynx  may  be  simultaneously  affected  with  motor  incoordination, 
and  then  the  speech  becomes  ataxic ;  the  articulation  is  hurried,  stutter- 
ing, and  becomes  so  indistinct  in  advanced  cases  that  the  patient's 
speech  is  almost  incomprehensible.  One  side  of  the  face  may  become 
suddenly  more  or  less  paralyzed,  and  paralysis  of  the  veil  of  the  palate, 
implicating  the  muscles  supplied  by  either  the  facial  or  glosso-pharyn- 
geal  nerves,  has  occasionally  been  observed,  while  the  symptoms  of 
bulbar  paralysis  have  been  known  to  occur  suddenly  in  the  early  stage 
of  ataxia.  These  paralyses  are,  like  the  corresponding  affections  of  the 
ocular  muscles,  generally  of  a  transitory  character. 

The  disorders  in  the  area  of  distribution  of  the  tenth  and  eleventh 
nerves  are  very  numerous,  and  give  to  the  disease  some  of  its  char- 
acteristic featuies. 

Laryngeal  crises,  consisting  of  paroxysms  of  spasmodic  cough  like 


518  DISORDERS    OF    MOTOR    CO  -  ORDINATION . 

those  of  whooping  cough,  are  liable  to  complicate  the  early  stage  of 
tabes,  while  paralysis  of  the  adductors,  or  more  rarely  of  the  abductors, 
of  the  vocal  cord  is  occasionally  present. 

Cardiac  crises,  consisting  of  paroxysms  of  angina  with  irregular 
and  frequent  pulse,  are  occasionally  present,  and  Charcot  believes  that 
in  ataxia  the  pulse  is  permanently  accelerated,  often  beating  from  100 
to  130  in  a  minute.  Aortic  regurgitation  has  so  frequently  been  found 
associated  with  locomotor  ataxia  that  some  authors  have  been  led  to 
believe  that  the  two  diseases  are  related  by  some  causal  connection. 

The  twelfth  nerve  is  only  rarely  affected  in  locomotor  ataxia,  but  it 
is  implicated  with  the  facial  and  laryngeal  nerves  when  there  is  ataxic 
speech.  Several  cases  of  tabes  are  recorded  in  which  the  lateral  half 
of  the  tongue  was  paralyzed  and  atrophied,  this  symptom  being  gener- 
ally associated  with  some  degree  of  atrophy  of  the  muscles  of  the  hand. 

{e)  Disorders  of  the  Visceral  Functions. — G-astrahjic  attacks  or  gas- 
tric crises  are  frequently  observed  in  the  premonitory  stage  of  tabes. 
The  attack  begins  suddenly  during  a  paroxysm  of  the  lancinating  pains. 
It  consists  of  severe  epigastric  pain,  which  radiates  in  different  directions, 
and  is  accompanied  by  distressing  vomiting  of  a  large  quantity  of 
watery  mucus,  which  ultimately  becomes  mixed  with  bile  and  blood. 
The  patient  suffers  during  the  attack  from  a  profound  malaise  and 
vertigo,  while  in  addition  to  the  gastric  pains  the  lancinating  pains  in 
the  extremities  are  unusually  severe  and  agonizing.  These  attacks 
may  last  for  two  or  three  days,  and  may  recur  every  two  weeks,  but 
usually  the  interval  between  them  is  not  less  than  a  month. 

Enteralgic  attacks  are  occasionally  present  in  tabes,  but  much  less 
frequently  than  the  gastric  crises.  These  attacks  consist  of  paroxysms 
of  unusually  severe  colic,  which  are  often  accompanied  l)y  diarrhocic 
crises,  or  painful  discharges  from  the  bowels  of  large  quantities  of 
watery  mucus  often  mixed  with  blood. 

Nephralgic  attacks,  the  symptoms  of  which  are  almost  in  every  respect 
similar  to  those  of  renal  colic  have  been  observed  in  tabes  in  the 
absence  of  calculi,  gravel,  or  blood  in  the  urine. 

Affections  of  the  Bladder  and  Rectum. — During  the  early  stage  of 
the  disease  the  patient  often  suffers  from  fre(iuent  and  painful  micturi- 
tion along  with  neuralgic  pains  in  the  depth  of  the  pelvis,  the  perineum, 
the  neck  of  the  bladder,  or  along  the  urethra.  At  other  times  the 
bladder  manifests  great  tolerance  of  its  contents,  most  probably  from 
some  degree  of  anaesthesia  of  the  mucous  membrane,  and  the  patient 
may  then  go  a  whole  day  without  feeling  any  desire  to  evacuate  his 
bladder,  and  when  he  empties  it  at  night  as  a  matter  of  routine  he  is 
surprised  at  the  large  quantity  it  contains.      At  a  later  stage  of  the 


PROGRESSIVE    LOCOMOTOR    ATAXIA.  519 

disease  paresis  of  the  bladder  makes  its  appearance,  so  that  emptvino- 
the  bladder  takes  an  unusually  lono;  time,  and  there  is  some  dribbling 
afterwards,  or  there  may  be  a  moderate  degree  of  incontinence,  but 
complete  paralysis  of  the  bladder  only  occurs  in  the  last  stage  of  the 
disease.  Dr.  Buzzard  has  suggested  that  a  phosphatic  calculus  may 
readily  form  in  tabes  with  bladder  troubles,  and  he  believes  that  many 
cases  of  atony  of  the  bladder,  for  which  surgeons  are  consulted,  are 
examples  of  talies. 

Patients  complain  in  the  early  stages  of  tabes  of  peculiar  sensations 
in  the  rectum  ;  they  sometimes  feel  as  if  a  large  foreign  body  were  being 
forcibly  introduced  in  the  anus,  and  this  sensation  is  accompanied  by  a 
strong  desire  to  evacuate  the  contents  of  the  bowel,  while  occasionally 
there  may  be  an  involuntary  discharge  of  fecal  matters.  Anaesthesia 
of  the  anus  and  paralysis  of  the  sphincter  are,  however,  only  present  in 
the  later  stages  of  the  disease. 

The  disorders  of  the  sexual  functions  consist  at  first  of  the  phenomena 
of  irritation,  but  even  from  the  beginning  the  voluptuous  sensations  are 
often  accompanied  by  slight  dribbling  of  urine,  spermatorrhoea,  and 
involuntary  seminal  emissions,  while  the  erections  are  often  imperfect 
and  accompanied  by  premature  ejaculation.  Locomotor  ataxia  in  women 
is  sometimes  ushered  in  by  symptoms  of  genital  irritation  arising  in  the 
absence  of  the  usual  sexual  excitants,  and  consisting  of  erections  of  the 
clitoris  followed  by  a  discharge  of  mucus. 

(/)  Vaso-motor  and  Trophic  Disturbances. — Yaso-motor  disorders 
are  not  prominent  features  of  locomotor  ataxia.  They  are  manifested 
by  the  presence  of  hot  or  more  frequently  cold  feet,  a  tendency  to  the 
formation  of  cutis  anserina^  mottling  of  the  skin,  increased  or  diminished 
cutaneous  secretion,  and  the  occurrence  of  patches  of  ecchymoses  on 
the  lower  extremities  during  paroxysms  of  severe  lancinating  pains. 

The  most  common  trophic  affections  are  cutaneous  eruptions,  such 
as  herpes,  lichen,  or  bullre  like  those  of  pemphigus,  these  eruptions 
sometimes  appearing  during  or  after  every  aggravated  attack  of  lancinat- 
ing pains.  The  nails  of  the  great  toes  are  liable  to  fall  off  spontaneously 
during  the  course  of  tabes,  and  are  replaced  in  a  few  weeks  by  ncAv  and 
perfectly  normal  nails,  which  may  in  their  turn  be  shed  a  few  months 
later,  and  this  process  may  be  repeated  several  times  in  succession.  All 
the  teeth  have  been  known  to  fall  out  w^ithin  a  period  of  a  few  weeks  in 
the  course  of  tabes.  Perforating  ulcer  of  the  foot  is  most  commonly 
met  wuth  in  subjects  who  are  suffering  from  the  earlier  symptoms  of 
tabes.  The  nutrition  of  the  muscles  is  usually  preserved  until  a  late 
period  of  the  disease,  but  occasionally  some  muscular  groups  may  undergo 
active  atrophy  in  the  preataxic  stage.     The  intrinsic  muscles  of  the 


520  DISORDERS    OF    MOTOR    CO-ORDINATION, 

hand  are  particularly  liable  to  be  attacked,  and  then  the  hand  presents 
the  well-known  claw-form,  but  the  muscular  atrophy  which  complicates 
tabes  does  not  pursue  the  progressively  invading  course  of  that  observed 
in  progressive  muscular  atrophy.  Atrophy  of  the  muscles  of  the  hand 
in  tabes  has  several  times  been  found  associated  with  hemiatrophy  of  the 
tongue. 

Disorders  in  the  Nutrition  of  Joints  and  Bones. — The  arthropathies 
des  ataxiques  of  Charcot  is  the  most  remarkable  trophic  affection  which 
is  met  with  in  tabes.  The  joint  affections  always  appear  in  the  loAver 
extremities  during  the  early  stage  of  tabes,  and  also  in  the  upper  ex- 
tremities during  the  early  invasion  of  the  symptoms  in  them,  although 
the  symptoms  may  be  long  established  in  the  lower  extremities,  and  they 
also  begin,  almost  always,  during  an  unusually  severe  paroxj^sm  of  lan- 
cinating pains.  The  knee-joint  is  the  one  most  frequently  affected,  and 
then  in  a  descending  order  of  frequency  the  shoulder,  elboAV,  hip-joint, 
wrist,  and  the  small  joints  of  the  feet  and  hands.  Various  luxations 
of  the  joints  ensue,  which  produce  notable  deformities  which  need  not  be 
described  here.  The  bones  sometimes  become  abnormally  friable,  so 
that  spontaneous  fractures  are  liable  to  occur. 

[g)  Cerebral  and  Psychical  Disorders. —  Vertigo  is  a  common  symp- 
tom of  the  early  stage  of  ataxia.  This  symptom  is  sometimes  the 
subjective  correlative  of  diplojiia,  or  is  associated  with  aural  troubles, 
but  occasionally  it  comes  on  in  the  absence  of  apparent  cause.  Essential 
vertigo  is  frequently  accompanied  by  confusion  of  mind,  an  involuntary 
turning  of  the  head  and  eyes,  and  an  eml)arrassment  of  speech  which 
sometimes  consists  of  a  difficulty  of  articulation  and  at  other  times  of 
a  decided  aphasia.  These  attacks  are  doubtless  of  the  nature  of  minor 
attacks  of  epilepsy,  and  we  shall  now  see  that  locomotor  ataxia  is  occa- 
sionally ushered  in  by  more  decided  epileptiform  attacks. 

Epileptiform  Attacks. — The  symptoms  of  tabes  may  be  ushered  in 
by  unilateral  epileptiform  attacks  with  subsequent  transitory  paralysis 
of  the  convulsed  limbs,  while  at  other  times  the  seizures  are  like  the 
petit  mal  or  occasionally  like  the  haut  nial  of  idiopathic  epilepsy. 

Apoplectiform  Attacks. — Locomotor  ataxia  may  also  be  preceded  or 
accompanied  by  apoplectiform  attacks  similar,  in  every  respect,  to  those 
which  are  met  Avith  in  sclerosis  in  patches  and  general  paralysis  of  the 
insane.  In  some  of  these  attacks  there  is  only  a  transitory  loss  of  con- 
sciousness from  whicli  the  patient  recovers  without  any  other  symptom  ; 
in  other  cases  the  seizure  is  accompanied  by  embarrassment  of  speech, 
facial  paralysis,  brachial  monoplegia,  or  complete  hemiplegia  with  or 
without  hemianeesthesia.  In  these  cases  the  recovery  takes  place  in  a 
few  hours  or  at  most  in  a  few  weeks,  the  transitory  nature  of  the  paral- 


PROGRESSIVE    LOCOMOTOR    ATAXIA.  521 

ysis  showing  that  it  must  have  resulted  from  a  functional  lesion  and  not 
from  a  hemorrhage  or  other  gross  lesion  of  the  brain.  Locomotor 
ataxia  may  also  be  complicated  with  a  permanent  hemiplegia,  and  in 
such  cases  care  should  be  taken  lest  the  ataxia  may  not  be  entirely  over- 
looked. 

Psychical  disorders  are  occasionally  observed  in  the  early  stao-e  of 
locomotor  ataxia  ;  the  patient  becomes  irritable  and  moody  and  towards 
the  end  of  the  disease  he  may  suffer  from  hallucinations,  illusions,  and 
weakness  of  memory.  At  other  times  his  moral  character  undergoes  a 
great  change ;  he  is  sometimes  grossly  indecent,  and  may  be  guilty  of 
making  lascivious  gestures,  or  leaving  his  clothes  unbuttoned  in  the 
presence  of  his  family.  The  symptoms  of  progressive  paralysis  of  the 
insane  are  frequently  associated  with  those  of  tabes,  and  sometimes  those 
of  the  former  and  sometimes  those  of  the  latter  take  the  precedence  in 
the  order  of  development. 

(2)  The  Ataxic  Stage. 

After  one  or  more  of  the  premonitory  symptoms  which  have  just 
been  described  have  been  in  existence  for  some  time,  the  phenomena 
which  characterize  the  ataxic  period  of  the  disease  make  their  appear- 
ance. The  duration  of  the  preataxic  stage  varies  greatly  in  different 
cases ;  in  exceptional  cases  the  ataxic  gait  begins  at  once,  while  in 
other  cases  lightning  pains,  amaurosis,  absence  of  patellar  tendon- 
reactions,  and  other  symptoms  of  the  disease  may  be  in  existence  for  a 
period  of  from  twenty  to  thirty  years  before  the  motor  incoordination 
is  fully  established. 

Static  Ataxia. — The  motor  disorders  of  tabes  almost  always  begin 
in  the  lower  extremities,  and  are  at  first  so  slight  that  they  can  only  be 
recognized  by  the  application  of  special  tests.  If  the  patient  be  asked  to 
stand  up  and  keep  his  feet  closely  applied  along  their  inner  edges,  he 
may  manage  to  maintain  the  erect  posture  with  moderate  steadiness  Avhen 
his  eyes  are  open,  but  when  they  are  closed  the  patient  immediately 
oscillates  from  side  to  side,  and  will  fall  unless  he  is  supported  or  open 
his  eyes.  A  still  severer  test  is  afforded  by  asking  the  patient  to  stand 
on  one  leg,  first  with  eyes  open  and  then  closed. 

As  the  muscular  incoordination  increases  standing  Avithout  support, 
even  when  the  eyes  are  open,  becomes  increasingly  difficult  and  finally 
impossible.  When  the  patient  now  stands  with  the  aid  of  two  sticks 
it  may  be  observed  that  all  the  extensor  muscles  of  the  body  are  in  a 
state  of  powerful  muscular  contraction.  The  muscles  of  the  calf  are 
strongly  contracted,  and  extend  the  leg  upon  the  foot  so  tliat  they  form 


522  DISORDERS    OF    MOTOR    CO-ORDINATION. 

an  obtuse  angle  with  one  another,  the  extensors  of  the  thigh  are  con- 
tracted and  extend  the  thigh  upon  the  leg,  the  flexors  of  the  thigh  are 
also  contracted,  and  the  foot  being  fixed  they  tend  to  extend  the  trunk 
on  the  thigh,  this  tendency  being  greatly  increased  by  contraction  of 
the  gluteal  muscles  and  of  the  erector  sp'mx.  The  tendency  of  the 
patient  to  fall  backwards,  caused  by  contraction  of  the  extensor  muscles, 
appears  to  be  counteracted  by  a  voluntary  contraction  of  the  muscles 
which  flex  the  body  upon  the  thighs.  The  body  is  thus  bent  forwards 
so  that  the  line  of  gravity  falls  in  front  of  the  line  joining  the  centres 
of  the  arches  of  the  feet,  and  the  tendency  to  fall  forwards  is  counter- 
acted by  the  support  of  the  two  sticks.  The  attitude  assumed  by  the 
patient  under  these  circumstances  is  characteristic.  The  feet  are  kept 
widely  apart  in  order  to  widen  the  base,  the  legs  are  drawn  backwards 
so  as  to  form  an  obtuse  angle  with  the  feet,  the  thighs  are  extended  on 
the  legs,  and  a  plumb-line  let  fall  from  each  trochanter  fiills  considera- 
bly behind  the  heel,  the  body  is  inclined  well  forwards  in  order  to  keep 
the  line  of  gravity  in  front  of  the  arches  of  the  feet,  and  the  buttocks 
project  well  backwards. 

Ataxic  G-ait. — In  the  early  stage  of  tlie  disease  the  patient  nuiy 
continue  to  walk,  when  once  he  has  started,  without  the  slightest  diffi- 
culty or  sign  of  motor  disorder,  but  he  may  be  observed  to  stagger  a 
little  on  getting  up  suddenly  from  a  chair,  especially  after  sitting  for 
some  time.  X  little  uncertainty  of  gait  may  also  be  observed  when  he 
is  asked  to  stop  walking  at  a  given  signal,  and  he  may  manifest  a  de- 
cided stagger  when  in  the  course  of  a  brisk  walk  he  is  asked  to  turn 
abruptly  around.  The  uncertainty  of  gait  is  also  increased  when  the 
patient  walks  in  the  dark  or  closes  his  eyes,  when  he  is  made  to  ascend 
or  descend  stairs,  or  when  he  walks  backwards. 

But  when  the  ataxia  becomes  more  j)ronounced  the  gait  is  so  charac- 
teristic that  it  can  be  readily  recognized  without  the  application  of 
any  special  tests.  The  patient  has  now  to  direct  his  eyes  to  the  ground 
and  to  his  feet  while  walking,  and  were  he  to  close  them  the  movements 
of  the  legs  would  become  disorderly,  and  walking  would  be  impossible. 
The  attitude  already  described,  with  the  tonic  contractions  of  the  ex- 
tensors of  the  body,  renders  it  impossible  for  the  foot  to  advance  Avith  the 
usual  pendulum  movement  of  healthy  locomotion ;  the  passive  foot  is 
flung  forwards  and  outwards  in  one  piece  with  a  rapid  jerk  by  a  simul- 
taneous contraction  of  the  flexors  of  the  thigh  on  the  body  and  the 
abductors  of  the  thigh,  and  it  is  subsequently  brought  to  the  ground 
with  a  thump.  During  the  advance  of  the  foot  the  heel  is  said  by 
some  observers  to  be  the  last  to  leave  the  ground  and  the  first  to  touch 
it  as  the  forward  movement  is  being  completed,  but  this  mode  of  pro- 


PROGRESSIVE    LOCOMOTOR    ATAXIA.  523 

gression  must  be  rare  if  it  ever  occurs.  "When  the  foot  is  about  to  be 
advanced  a  certain  degree  of  flexion  occurs  at  the  knee-joint  and  the  foot 
is  raised  oft'  the  ground:  the  foot  is  then  suddenly  projected  forwards 
and  outwards,  and  the  heel  is  afterwards  brought  down  with  a  thump 
in  the  manner  ah-eady  described.  In  order  to  enable  the  passive  leo-  to 
clear  the  ground  during  its  forward  movement,  the  abductor  muscles  of 
the  thigh  on  the  side  of  the  active  leg  enter  into  strong  contraction, 
and  the  pelvis  on  the  side  of  the  passive  leg  is  thus  well  elevated. 
The  elevation  of  the  pelvis  on  the  side  of  the  passive  leg  is  indeed  so 
well  marked  that  the  patient  is  in  some  danger  of  carrying  his  centre 
of  gravity  too  far  to  the  side  of  the  active  leg.  In  order  to  counteract 
this  tendency  the  upper  part  of  the  body  is  curved  to  the  opposite  side 
by  contraction  of  the  erector  spinse,  and  when  the  patient  is  able  to 
walk  without  the  aid  of  sticks  the  arm  on  the  side  of  the  passive  leg  is 
thrust  out  laterally,  and,  in  order  to  maintain  his  equilibrium  during 
the  transference  of  the  line  of  gravity  from  one  foot  to  the  other  in 
walking,  the  trunk  is  strongly  inclined  from  one  side  to  the  other,  and 
the  arms  are  flung  about  like  those  of  a  rope-dancer.  When  the  patient 
walks  by  the  aid  of  sticks,  the  tendency  to  too  great  a  displacement  of 
the  line  of  gravity  towards  the  side  of  the  active  leg  is  instinctively 
counteracted  by  an  outward  inclination  being  given  to  the  sticks,  so 
that  they  aff'ord  a  lateral  support. 

Patients  have  been  known  to  walk  long  distances  after  being;  aifected 
with  a  high  degree  of  ataxia,  but  after  a  time  the  incoordination 
becomes  so  great  that  the  maintenance  of  the  erect  position  and  walking 
become  impossible.  If  the  patient  be  now  supported  by  two  persons 
under  the  arms  whilst  he  tries  to  walk,  the  legs  are  thrust  backwards 
and  forwards,  to  the  right  and  to  the  left  in  the  utmost  disorder,  and 
are  incapable  of  giving  the  least  support  to  the  body :  they  move,  as 
Trousseau  remarks,  like  those  of  a  puppet  or  a  marionette.  The 
muscles  of  the  trunk  now  become  affected,  and  the  body  makes  irregular, 
swaying  movements  when  the  patient  sits  in  a  cliair,  but  even  in  these 
advanced  cases  the  patient  when  laid  doAvn  may  be  able  to  resist  passive 
movements  of  the  limbs,  and  to  perform  the  simple  movements  of  flexion 
and  extension  w'ith  scarcely  diminished  poAver.  When  the  patient  now 
attempts  to  touch  an  object  with  the  tip  of  the  foot,  the  line  of  motion 
is  irregular  and  zigzaw,  and  disturbed  by  lateral  movements,  while  he 
is  quite  incapable  of  exerting  more  complicated  movements,  such,  for 
•instance,  as  are  required  in  describing  an  imaginary  circle  with  the  tip 
of  the  great  toe. 

At  a  late  period  the  ataxia  appears  in  the  upper  extremities ;  in  the 
cases  of   hereditarv   ataxia   described  by   Friedreich,   the  motor  inco- 


524  DISORDEES    OF    MOTOR    CO  -  ORDINATION . 

ordination  appears  in  the  npper  simultaneously  with,  or  soon  after  its 
first  manifestation  in  the  lower  extremities,  but  in  the  more  usual  form 
of  the  disease  ataxia  of  the  upper  extremities  is  rare  and  belongs  to  the 
later  manifestations  of  the  disease.  In  ataxia  of  the  upper  extremities, 
complicated  and  special  movements,  such  as  those  required  for  writing 
or  playing  the  piano,  are  uncertain,  and  the  irregularity  becomes  greater 
if  an  attempt  is  made  to  perform  them  Avith  closed  eyes.  The  slighter 
degrees  of  ataxia  of  the  upper  extremities  may  be  tested  by  instructing 
the  patient  to  touch  with  closed  eyes  some  part  of  the  surface  of  the  body, 
such  as  the  tip  of  the  nose  or  lobule  of  one  ear  with  the  point  of  the  fore- 
finger of  each  hand  alternately,  Avhen  the  ataxia  declares  itself  by  the 
inability  of  the  patient  to  touch  the  intended  spot  until  after  repeated 
trials.  A  similar  uncertainty  is  observed  when  the  patient  is  asked  to 
transfer  a  small  object  from  one  hand  to  the  other.  At  a  later  period 
of  the  disease  the  simpler  movements  become  irregular  and  ataxic, 
the  patient  fumbles  in  buttoning  and  unbuttoning  his  clothes,  the  act  of 
grasping  is  performed  in  an  uncertain  and  spasmodic  manner,  and  the 
patient  can  only  reach  the  object  in  a  roundabout  way  and  with  jerky 
interruptions.  Static  ataxia  may  be  revealed  in  the  upper  extremities 
by  the  inability  of  the  patient  to  hold  out  his  arms  horizontally,  especi- 
ally when  the  eyes  are  closed.  In  a  still  more  advanced  stage  of  the 
disease  patients  can  no  longer  dress  or  feed  themselves,  inasmuch  as 
they  cannot  perform  such  simple  movements  as  are  requisite  for  carry- 
ing a  spoon  to  the  mouth,  but  even  under  these  circumstances  they 
may  be  able  to  exert  great  muscular  power  in  resisting  passive  move- 
ments. The  ataxy  may  invade,  as  we  have  seen,  the  muscles  of  the 
trunk,  and  ultimately  the  muscles  of  the  neck  may  also  be  implicated, 
and  the  head  is  the  subject  of  irresular  and  shakinjr  movements. 

The  electrical  reactions  of  the  muscles  are  not  of  much  value  in  the 
prognosis  or  diagnosis  of  locomotor  ataxia.  It  is  probable  that  in  the 
earlier  stages  of  the  disease  there  is  an  increase  and  in  the  later  stages 
a  diminution  of  the  electric  contractility. 

Sensory  Disorders. — The  girdle  pains  and  the  lightning  pains  of 
the  premonitory  period  are  continued,  as  a  rule,  through  the  ataxic 
stage,  and  often,  indeed,  become  increased  in  severity  as  the  disease 
advances.  The  hyperaesthetic  spots,  however,  now  give  place  to  anaes- 
thesia, and  an;^sthetic  patches  may  be  found  on  the  soles  of  the  feet, 
the  toes,  and  the  back  of  the  feet,  and  they  may  become  widely  diffused 
over  the  thighs  and  trunk  before  the  patient  is  aware  of  their  presence. 
After  a  time,  however,  the  patient  finds  that  he  no  longer  feels  the  floor 
distinctly,  that  all  articles  which  he  touches  have  a  velvety  feel,  and 
that  he  cannot  hold  small   objects  in  his  fingers.     Every  variety  of 


PROGEESSIVE    LOCOMOTOR    ATAXIA.  525 

paralysis  of  sensation  and  every  combination  of  these  are  met  with  in 
the  late  stages  of  the  affection,  but  probably  analgesia  is  the  most 
frequent.  Occasionally,  however,  the  sensibility  to  pain  is  retained,  or 
even  increased,  while  there  is  a  diminution  of  sensibility  to  some  or  all 
\arieties  of  touch,  and  again,  partial  paralysis  of  the  sense  of  touch 
may  be  combined  with  analgesia  and  hyperalgesia,  or  with  hypera;s- 
thesia  towards  impressions  of  temperature.  At  a  late  period  of  the 
lisease  a  distinct  retardation  of  the  conduction  of  sensations,  especialh^ 
■A'  impressions  of  pain,  is  observed,  and  this  may  also  be  found  in  the 
earlier  stages.  The  prick  of  a  pin  frequently  gives  rise  to  a  double 
sensation,  the  first  of  touch  and  the  second  of  pain,  and  the  sense  of 
temperature  may  also  be  retarded.  The  sensation  of  pain  continues 
fi)r  a  relatively  long  time,  even  when  its  cause  has  only  been  of 
momentary  duration,  and  the  highest  degree  is  not  reached  until  several 
seconds  after  the  pain  has  begun.  In  circumscribed  areas  of  the  skin 
of  the  foot  the  patient  may  feel  two  points  when  only  one  is  touching 
the  skin,  and  when  two  points  are  in  contact  four  or  five  may  be  felt. 
In  some  cases  the  patient  is  not  sure  which  side  of  the  body  is  touched 
when  the  eyes  are  closed,  even  although  the  cutaneous  sensibility  is 
more  or  less  completely  retained.  In  the  early  stage  of  the  disease 
the  disorders  of  the  muscular  sensibility  and  muscular  sense  declare 
themselves  by  a  feeling;  of  fatigue  and  the  sensation  termed  the 
"fidgets,"  but  as  the  disease  advances  the  muscular  sense  becomes 
diminished,  and  consequently  the  power  of  recognizing  what  muscles 
are  thrown  into  action  is  lessened  in  a  corresponding  degree.  After  a 
time  the  patient,  when  his  eyes  are  closed,  cannot  tell  the  position  of 
his  lower  extremities,  and  has  lost  the  power  of  recognizing  small 
weights,  and  of  discriminating  the  differences  of  Aveights. 

Visceral  Disorders. — The  gastralgise  are  seldom  so  distressing  in  the 
second  as  in  the  first  stage  of  the  disease,  but  the  genito-urinary  symp- 
toms become  much  more  urgent  and  troublesome.  The  sexual  weak- 
ness of  the  early  stage  now  advances  to  complete  impotence,  and  the 
dribbling  of  urine,  which  was  at  first  an  occasional  symptom,  now 
becomes  habitual,  while  in  some  cases  there  is  so  much  antesthesia  of 
the  urethra  that  the  urine  may  pass  in  a  full  stream  without  the  patient's 
knowledge.  In  other  cases  the  patient  is  unable  to  evacuate  the  l)lad- 
der,  Avhich  becomes  so  distended  as  to  require  the  use  of  the  catheter. 
The  tenesmus  and  neuralgiform  pains  about  the  rectum,  which  were 
present  in  the  first  stage  of  the  disease,  now  give  place  to  anaesthesia, 
and  then  there  may  be  an  unconscious  passage  of  the  stools,  which, 
indeed,  would  be  a  much  more  frequent  symptom  if  it  was  not  for  the 
high  degree  of  constipation  which  is  usually  present. 


526  DISORDERS    OF    MOTOR    CO  -  O  RDIN  ATIOX  . 

Trophic  disorders  are  not  liable  to  occur  in  this  stage  of  the  disease, 
but  the  skin  of  the  lower  extremities  may  become  dry  and  covered  by 
furfuraceous  scales,  and  patches  of  ichthyosis  may  form  over  the  toes 
and  metatarsal  bones,  and  the  muscles  of  the  lower  extremities  may 
noAV  undero-o  diffused  Avastino-. 


(3)  The  Paralytic  Staue. 

In  the  terminal  period  of  locomotor  ataxia  the  motor  incoordination 
has  increased  to  such  an  extent  that  the  patient  is  quite  unable  to  walk, 
and  he  is  consequently  obliged  to  sit  propped  up  in  an  armchair,  or  to  lie 
helplessly  in  bed ;  but  even  when  he  is  quite  unable  to  stand,  the  indi- 
vidual movements  of  the  lower  extremities  may  be  performed  with 
scarcely  diminished  power.  But  after  a  time  even  the  power  of  per- 
forming separate  movements  is  diminished,  and  the  muscles  undergo 
diffused  atrophy,  are  soft  and  flaccid,  and  no  tension  is  provoked  on 
passive  movements  of  the  limbs.  The  anaesthesia  to  pain  and  touch  is 
now  complete,  the  patient  is  quite  unable  to  tell  the  position  of  his  limbs 
in  bed  without  the  aid  of  sight ;  but  the  sense  of  temperature  may  still 
remain  nearly  normal.  The  patient  also  suffers  from  incontinence  of 
urine  ;  the  stools  pass  unconsciously  ;  bedsores  appear  on  the  sacrum  ; 
chronic  cystitis  supervenes ;  and  the  patient  dies  in  a  state  of  great 
marasmus,  as  in  other  forms  of  myelitis.  In  other  cases  the  disease  ma}'' 
progress  ujiwards  and  implicate  the  medulla  oblongata,  and  the  patient 
dies  from  respiratory  troubles,  or  diflSculties  of  deglutition.  At  other 
times  cerebral  symptoms  may  supervene,  and  the  patient,  after  being 
delirious  for  a  few  days,  dies  comatose.  But  the  disease  runs  its  full 
course  only  on  rare  occasions,  and  in  the  majority  of  cases  the  patient 
dies  from  an  intercurrent  disease  such  as  acute  pneumonia,  phthisis, 
or  cardiac  complication.  The  course  of  locomotor  ataxia  is  usually  slow 
and  chronic  ;  it  often  extends  over  a  period  of  many  years,  and  even  the 
initial  stage,  with  lancinating  pains,  may  last  more  than  twenty  years.  In 
the  majority  of  typical  cases  the  average  duration  of  life  appears  to  be 
from  eight  to  twelve  years,  but  a  few  cases  run  a  rapid  course,  these 
having  been  described  under  the  name  of  acute  ataxia. 

Varieties. — The  following  clinical  varieties  of  locomotor  ataxia  may 
be  distinguished : 

(1)  The  typical  form  of  tabes,  which  begins  with  lancinating  and  girdle 
pains,  loss  of  patellar  tendon-reactions,  and  disorders  of  the  oculo- 
motor nerves,  and  runs  through  the  preataxic,  ataxic,  and  paralytic 
stages  which  have  been  described. 


PEOGRESSIVE    LOCOMOTOR    ATAXIA.  527 

(2)  Hereditary  Tabes. — This  form  of  tabes  was  first  described  by 
Friedreich.  The  disease  begins  between  the  ages  of  twelve  and  eighteen 
years ;  it  is  usually  remarkably  protracted,  extending  sometimes  over  a 
period  of  thirty  years ;  several  members  of  the  same  family  are  liable 
to  be  affected,  and  the  female  members  appear  to  be  attacked  by  prefer- 
ence. Lancinating  pains  and  other  sensory  disorders  are  never  well 
marked  and  are  often  absent ;  the  ataxia  begins  at  an  early  period  and 
attacks  the  upper  extremities  simultaneously  with  or  soon  after  the  lower 
extremities.  Disorders  of  articulation,  and  ataxic  nystagmus  are 
generally  present,  and  the  tendon-reactions  are  lost ;  but  static  ataxia, 
bedsores,  psychical  disorders,  tremor,  and  amaurosis  are  generally  absent ; 
while  muscular  atrophy,  paresis,  contractures,  'and  weakness  of  the 
bladder  appear  only  in  the  last  stage.  The  symptoms  of  this  group 
are  very  variable  and  the  cases  included  in  it  are  probably  more  allied 
to  sclerosis  in  patches  than  to  locomotor  ataxia. 

(3)  Anomalous  Form. — This  variety  comprises  the  form  in  which 
are  present  arthropathies,  muscular  atrophy,  tremors  of  the  upper  ex- 
tremities, psychical  disorders,  or  any  other  prominent  symptom  which 
does  not  belong  to  the  typical  disease. 

(4)  Paraplegic  Form. — In  some  cases  the  symptoms  of  tabes  are 
obscured  by  the  presence  of  paraplegia.  The  presence  of  paralysis 
with  muscular  tension  may  lead  the  observer  to  believe  that  the  case  is 
one  of  ordinary  paraplegia,  but  in  such  cases  the  patellar  tendon-reac- 
tions are  usually  absent,  instead  of  being  exaggerated,  as  in  ordinary 
paraplegia.  These  cases  will  be  subsequentl}^  described  under  the  name 
of  posterior  and  lateral  sclerosis. 

(5)  Neuralgic  Form. — The  lancinating  pains  are  very  violent  and 
distressing  in  this  form,  and  these  pains  and  the  absence  of  the  patellar 
tendon-reactions  may  be  the  only  symptoms  present  for  upwards  of 
twenty  years,  and  consequently  this  variety  has  been  named  "  tahes 
dolorosa''  or  "abortive  locomotor  ataxia."  Amaurotic  tahes  belongs 
to  this  variety,  inasmuch  as  white  atrophy  with  blindness  may  exist  for 
very  many  years  without  any  other  symptom  except  absence  of  the 
patellar  tendon-reactions. 

(6)  Hemiataxia. — The  ataxic  symptoms  may  in  rare  cases  be  much 
more  pronounced  on  one  side  of  the  body  than  on  the  other. 

(7)  Meningitic  Form. — When  locomotor  ataxia  is  complicated  with 
spinal  meningitis  the  typical  symptoms  of  tabes  are  apt  to  be  compli- 
cated by  pain  in  the  back,  and  along  the  vertebral  column,  spinal 
tenderness,  and  diffused  or  circumscribed  cutaneous  hyperaesthesia. 


528  DISOEDEKS    OF    MOTOR    CO-ORDINATION, 

5.  COMBINED   SCLEROSIS   OF   THE    POSTERIOE   AND   LATERAL 

COLUMNS. 

Symptoms. — The  symptoms  of  locomotor  ataxia  and  of  primary 
lateral  sclerosis  may  be  present  in  every  possible  combination,  those  of 
the  former  disease  predominating  at  one  time  and  those  of  the  latter  at 
another. 

The  symptoms  Avhich  indicate  that  the  lateral  columns  are  being 
gradually  invaded  in  cases  of  locomotor  ataxia  are  spontaneous  jerkings 
in  the  lower  extremities,  gradual  loss  of  power  to  perform  simple  move- 
ments of  extension  and  flexion,  muscular  tension,  and  contractures. 
When  the  symptoms  of  lateral  sclerosis  predominate,  the  signs  ])y  which 
a  complication  of  locomotor  ataxia  may  be  suspected  are  the  presence 
of  lancinating  pains,  girdle  pains,  and  other  sensory  disturbances,  vesical 
Aveakness,  slight  swaying  on  closing  the  eyes,  and,  above  all,  the  absence 
of  the  patellar  tendon-reaction  and  ankle-clonus.  Two  cases  came 
under  my  observation  in  Avhich  the  symptoms  of  pure  lateral  sclerosis 
Avith  exaggerated  tendon-reactions  present  in  the  lower  extremities  were 
accompanied  by  extreme  myosis  of  both  pupils,  and  it  is  probable  that 
there  was  a  combination  of  sclerosis  of  the  lateral  columns,  and  of  the 
posterior  columns  in  the  upper  segment  of  the  cord. 


6.  DISEASES  OF  THE  CEREBELLUM. 

The  diseases  of  the  cerebellum  consist  of  hemorrhage,  abscess,  and 
tumors. 

Symptoms. — The  general  symptoms  of  cerebellar  disease  consist  of 
headache,  Avhich  is  more  frequently  situated  in  the  occiput  and  only 
occasionally  in  the  forehead,  vomiting,  vertigo,  unsteadiness  on  stand- 
ing Avhich  increases  Avhen  the  eyes  are  closed,  and  a  reeling  gait.  In 
hemorrhage  the  symptoms  come  on  suddenly,  and  when  a  large  clot 
forms  the  patient  suffers  from  apoplectic  symptoms,  and  death  may  occur 
rapidly  from  pressure  on  the  pons  and  medulla  oblongata.  Abscess  of 
the  cerebellum  generally  results  from  disease  of  the  middle  ear,  Avhile  a 
tumor  declares  itself  by  the  gradual  onset  of  the  symptoms  or  by  the 
presence  of  double  optic  neuritis,  Avhich  is  frequently  accompanied  by 
amblyopia  or  even  complete  blindness. 

Stationary  lesions  in  the  cerebellum  may  be  of  large  size  without 
giving  rise  to  any  recognizable  symptoms.  Progressive  lesions  cause 
different  symptoms  according  to  the  situation  of  the  lesion.  When  the 
lesion  is  situated  in  the  upper  part  of  the  middle  lobe  the  patient  has  a 


DISEASES    OF    THE    CEREBELLUM.  529 

Staggering  gait,  and  manifests  a  tendency  to  fall  backwards,  and  when 
it  is  situated  in  the  inferior  part  of  the  middle  lobe  it  is  probable  that 
the  tendency  is  to  fall  forwards,  or  to  revolve  round  a  horizontal  axis. 
Tumors  situated  near  the  upper  part  of  the  middle  lobe  give  rise  to  a 
tonic  contraction  of  the  muscles  of  the  neck  which  causes  retraction  of 
the  head.  The  muscles  of  the  trunk  and  extremities  may  likewise  be 
implicated  in  the  spasm,  and  the  patient  then  suffers  from  tetaniform 
seizures,  during  which  the  head  is  retracted,  the  body  arched  backwards, 
the  lower  extremities  extended,  and  the  upper  strongly  flexed  as  in  teta- 
nus. All  lesions  attended  with  an  increase  of  size,  like  abscesses  and 
tumors,  must  exert  pressure  forwards  on  the  pons,  inasmuch  as  the  or^an 
is  limited  above  by  the  unyielding  tentorium  and  behind  and  below  by 
the  occiptal  bones.  The  consequence  is  that  abscesses  and  tumors  of 
the  cerebellum  are  often  attended  by  slight  weakness  of  the  limbs  with 
increase  of  the  tendon-reactions.  The  long  course  of  the  sixth  nerves 
in  front  of  the  pons  to  reach  the  cavernous  sinus  renders  one  or  other 
of  them  liable  to  be  paralyzed  in  tumors  of  the  middle  lobe.  Cases  of 
tumor  of  the  middle  lobe  are  met  with  in  which  the  patellar  tendon- 
reactions  are  absent  without  any  disease  being  found  in  the  spinal  cord. 
It  is  possible  that  in  these  cases  there  is  an  increase  of  the  spinal  fluid, 
owing  to  obliteration  of  the  foramen  of  Magendie,  which  forms  the  com- 
munication between  the  spinal  and  cerebral  subarachanoid  spaces. 
Tumors  of  the  cerebellum  are  also  sometimes  attended  by  numbness  and 
tingling  of  the  trunk  and  extremities,  but  only  rarely  by  amTesthesia, 
and  one  or  more  of  the  cranial  nerves  may  be  more  or  less  paralyzed. 
Movements  of  the  eyeballs  are  frequently  observed  in  cases  of  tumor 
of  the  middle  lobe  of  the  cerebellum.  These  movements  may  be  ver- 
tical, horizontal,  or  oblique,  and  are  generally  parallel.  At  times  they 
are  only  observed  during  a  tetaniform  seizure,  but  Avhen  there  is  per- 
manent rigidity  the  eyes  may  be  rotated  in  one  direction  and  fixed,  or 
slight  parallel  oscillatory  movements  may  be  present.  When  the  lesion 
is  situated  in  one  of  the  lateral  lobes  or  in  one  of  the  middle  peduncles, 
there  is  a  tendency  to  fall  towards  the  side  of  the  lesion.  If  a  tumor 
is  growing  slowly,  the  tendency  to  fall  to  one  side  is  counteracted  by 
cerebral  action  to  such  an  extent  that  this  symptom  is  not  readily 
elicited,  but  when  the  patient  turns  suddenly  round,  especially  with 
closed  eyes,  a  slight  stagger  may  be  observed,  or  the  statement  of  the 
patient  may  indicate  to  which  side  he  has  a  tendency  to  fall.  A  tumor 
of  one  lateral  lobe  may  also  encroach  upon  the  middle  lobe,  and  then 
the  tendency  to  stagger  to  one  side  is  accompanied  by  a  tendency  to 
fall  backwards,  so  that  the  patient  now  manifests  an  inclination  to  fall 
backwards  and  to  one  side  in  a  diagonal  direction.     If  the  tumor  grows 

34 


530  DISORDERS    OF    MOTOR    CO-ORDINATION. 

forwards  so  as  to  encroach  upon  the  hiteral  half  of  the  pons,  some  of 
the  cranial  nerves  become  paralyzed,  while  the  sensory  and  motor  tracts 
may  be  more  or  less  compressed.  In  such  a  case  paralysis  of  the  sen- 
sory and  motor  branches  of  the  trigeminus  may  be  present  either  separ- 
ately or  combined,  along  with  more  or  less  hemiplegia  of  the  opposite  side. 
Much  more  frequently  the  patient  becomes  completely  deaf  on  the  side 
of  the  lesion  from  compression  of  the  auditory  nerve,  facial  paralysis  is 
then  established,  and  the  external  rectus  of  the  eyeball  is  the  last  to  be 
affected.  If  the  growth  begins  in  the  pons  the  sixth  or  seventh  nerves 
are  the  first  to  be  affected,  and  the  auditory  nerve  last.  If  the  growth 
encroaches  upon  the  pyramidal  tract  hemiplegia  of  the  opposite  side, 
with  or  without  some  degree  of  anaesthesia,  accompanies  deafness  and 
peripheral  facial  paralysis  on  the  same  side  as  the  lesion.  The  para- 
lytic phenomena  may  be  preceded  by  spasmodic  contractions  of  the 
masticatory,  facial,  or  ocular  muscles.  Instead  of  paralysis  of  the 
external  rectus  of  the  eyeball  on  the  side  of  the  lesion,  there  may  be  a 
conjugate  deviation  of  the  eyes,  which  is  directed  towards  the  diseased 
side  when  the  lesion  is  irritative,  and  away  from  it  when  it  is  destructive. 
The  symptoms  caused  by  lesion  of  the  inferior  peduncle  of  the  cere- 
bellum are  not  well  ascertained.  In  a  case  in  which  I  suspected  a 
hemorrhage  of  the  restiform  body  where  it  joins  the  inferior  peduncle, 
the  symptoms  were  paralytic  myosis  and  diminution  of  the  palpebral 
fissure,  and  partial  anaesthesia  of  the  face  on  the  side  of  the  lesion, 
and  partial  hemiplegia  with  well-marked  hemianesthesia  on  the  opposite 
side.  Although  the  patient  could  move  the  partially  paralyzed  limbs 
pretty  freely  in  bed,  he  was  totally  unable  to  stand  without  support ; 
he  had,  indeed,  to  be  supported  on  both  sides  in  order  to  be  kept  erect, 
and  it  seemed  as  if  he  had  an  equal  tendency  to  fall  backwards,  for- 
wards, and  to  either  side.  On  attempting  to  walk  the  head  was  drawn 
slightly  backwards,  and  the  eyes  were  directed  upwards,  the  body  was  in- 
clined to  the  paralyzed  side  until  it  was  at  an  angle  of  about  sixty  degrees 
to  the  floor,  and  as  each  foot  was  moved  forwards  it  was  raised  about 
eighteen  inches  from  the  ground,  and  the  patient  had  the  greatest  diffi- 
culty in  disentangling  it  from  the  leg  which  was  planted  on  the  ground. 
Sometimes  he  raised  the  feet  alternately  in  the  most  ridiculous  manner 
without  moving  forwards  at  all.  When  he  attempted  to  lie  down,  after 
being  placed  sitting  on  the  edge  of  the  bed,  his  head  became  rotated 
towards  the  side  of  the  lesion,  and  by  the  time  his  body  reached  the 
bed  his  face  was  directed  towards  the  pillow.  On  some  occasions  the 
patient  on  making  a  semi-revolution  round  his  longitudinal  axis,  worked 
his  way  back,  but  not  without  considerable  difficulty,  until  he  got  on  his 
back,  while  at  other  times  he  only  got  on  his  back  after  making  a  com- 


DISEASES    OF    THE    CEREBELLUM.  531 

plete  revolution.     He  never  manifested  a  tendency  to  revolve  on  his 
longitudinal  axis  when  once  laid  on  his  back. 

The  symptoms  caused  by  lesion  of  the  superior  peduncle  of  the  cere- 
bellum are  also  not  well  known.  The  proximity  of  these  peduncles  to 
the  corpora  quadrigemina  renders  it  probable  that  they  would  give  rise 
to  unilateral  or  bilateral  disorders  of  vision,  and  it  is  not  unlikely  that 
the  eyeballs  might  be  found  on  different  levels,  the  one  being  directed  a 
little  upwards  and  outwards,  and  the  other  a  little  downwards  and  out- 
wards. Lesions  in  this  situation  might  also  be  expected  to  give  rise  to 
disorders  of  the  third  nerve. 

Morbid  Anatomy. — In  aural  vertigo  the  lesion  was  thought  by 
Meniere  to  be  limited  to  the  semicircular  canal  and  vestibule,  but 
Knapp  thinks  that  all  parts  of  the  labyrinth  are  involved.  The  dis- 
ease of  the  labyrinth  may  be  primary  or  secondary  to  affections  of  the 
tympanic  or  cranial  cavity.  The  primary  affections  of  the  labyrinth 
are  (1)  hemorrhage  from  suppression  of  the  menses,  severe  attacks  of 
fever,  or  fractures  of  the  petrous  portion  of  the  temporal  bone ;  (2)  serous 
effusion  in  specific  forms ;  and  (3)  the  formation  of  pus  as  a  complica- 
tion of  purulent  meningitis.  When  aural  vertigo  is  an  early  symptom 
of  locomotor  ataxia  the  lesion  is  most  probably  a  parenchymatous 
neuritis  of  the  auditory  nerve.  The  secondary  diseases  of  the  labyrinth 
are  set  up  by  an  extension  to  it  of  inflammation  in  cases  of  acute  and 
chronic  catarrh  of  the  middle  ear.  All  that  is  known  of  the  morbid 
anatomy  of  primary  sclerosis  of  the  columns  of  Goll  has  been  men- 
tioned along  with  the  description  of  the  symptoms,  while  the  secondary 
sclerosis  of  these  columns  and  of  the  direct  cerebellar  tracts  has  already 
been  considered. 

In  locomotor  ataxia  the  spinal  pia  mater,  especially  in  the  posterior 
aspect  of  the  cord,  is  often  thickened,  cloudy,  and  connected  to  the 
dura  mater  by  numerous  adhesions,  while  the  spinal  fluid  is  increased. 
The  cord  is  generally  of  an  increased  consistence,  although  it  has  occa- 
sionally been  found  softened,  and  it  is  often  flattened  from  before  back- 
wards owing  to  the  atrophy  of  the  posterior  columns,  while  a  grayish- 
yellow  discoloration  may  be  observed  extending  the  whole  length  of 
the  cord  along  the  posterior  median  fissure.  On  making  transverse 
section  the  posterior  columns  are  seen  to  be  of  a  grayish  color  and 
diminished  in  size,  and  the  posterior  gray  horns  and  posterior  roots 
have  also  Ijeen  found  atrophied.  The  degeneration  is  not,  as  a  rule, 
uniformly  distributed  over  the  whole  transverse  area  of  the  posterior 
columns.  The  intensity  and  extent  of  the  lesion,  in  long-standing  cases, 
are  greatest  in  the  upper  lumbar  and  dorsal  regions,  when  it  occupies 
the  whole  transverse  section  of  the  posterior  columns.     In  the  inferior 


532 


DISORDEKS    OF    MOTOR    CO  -  ORDINATION 


portion  of  tlie  lumbar  region  there  is  frequently  only  a  slight  gray  dis- 
coloration in  the  external  half  of  the  posterior  columns,  while  in  the 
upper  dorsal  and  cervical  regions  the  area  of  the  lesion  becomes  again 
restricted,  and  in  the  upper  cervical  region  the  columns  of  Goll  are 
alone  affected.  In  long-standing  cases  the  posterior  gray  horns  may  be 
found  shrivelled  and  distorted,  and  the  posterior  roots  wasted,  while  the 
direct  cerebellar  tracts  may  likewise  be  affected,  and  in  a  few  cases  the 
anterior  gray  horns  have  been  implicated.  In  very  protracted  cases 
the  whole  transverse  area  of  certain  portions  of  the  cord  may  be  found, 
on  section,  transformed  into  a  gray  translucent  mass.     But  when  a 

Fig.  169. 


V^v 


A  ^ 

Teassverse  Section  of  the  LxniBAR  Region,  from  a  Case  of  Locomotok  Ataxia,  (.omplicated 

WITH   MuSCDLAtt  ATROPHY.      (CHARCOT  and  PlERRET.) 

A,  A,  Sclerosis  of  tlie  posterior  root-zone  ;  C,  Left  anterior  gray  horn,  healthy  ;  D,  Right  anterior 
gray  horn  in  a  state  of  atrophy 

patient,  suffering  from  lancinating  pains  and  other  symptoms  of  abor- 
tive tabes,  dies  from  some  intercurrent  disease,  the  sclerosis  is  limited 
to  the  root-zones  of  the  posterior  columns,  and  the  columns  of  Goll 
are  free  from  disease  (Fig.  1(39). 

On  microscopical  examination  of  the  portions  of  the  cord  which  have 
undergone  sclerosis,  the  interstitial  tissue  is  found  increased  in  amount, 
the  nuclei  and  Deiter's  cells  are  increased  in  number,  the  walls  of  the 
vessels  are  thickened,  and  corpora  amylacea  and  granule  cells  are  scat- 


DISEASES    OF    THE    CEREBELLUM.  533 

tered  tliroughout  the  tissue,  the  nerve  fibres  are  thin  and  wasted,  and 
many  of  them  have  disappeared,  while  in  the  later  stages  of  the  disease 
the  tissue  is  converted  into  a  firm  fibrillary,  often  wavy  connective 
tissue,  in  which  only  a  few  traces  of  nerve  fibres  are  left. 

The  ganglion  cells  of  the  posterior  gray  horns  are  often  found  pig- 
mented, but  the  ganglion  cells  in  Clarke's  columns  are  unaffected  although 
a  number  of  fine,  apparently  degenerated,  nerve  fibres  may  be  seen  to 
pass  through  and  around  them.  The  degenerative  process  sometimes 
extends  to  the  anterior  gray  horns,  and  the  motor  ganglion  cells  and 
anterior  roots  are  then  seen  to  be  atrophied.  Degenerative  changes 
have  likewise  been  discovered  in  the  peripheral  nerves  and  the  posterior 
roots,  and  cases  have  recently  been  recorded  which  render  it  probable 
that  the  morbid  changes  of  tabes  begin  in  the  afferent  fibres  of  the 
peripheral  nerves.  The  optic  nerves  are  sometimes  found  atrophied, 
and  morbid  changes  have  occasionally  been  found  in  the  ocular  motor 
and  hypo-glossal  nerves,  while  the  roots  of  the  pneumogastric  nerves 
have  been  found  atrophied  in  cases  of  tabes  Avith  laryngeal  crises.  The 
nuclei  of  origin  of  the  cranial  nerves  on  the  floor  of  the  fourth  ventricle 
and  the  floor  of  the  aqueduct  of  Sylvius  are  occasionally  involved  in 
the  disease.  When  arthropathies  form  part  of  the  disease  the  articular 
cartilages  of  the  affected  joints  are  destroyed,  while  the  articular  ends 
of  some  of  the  bones  are  eroded.  In  cases  of  combined  lateral  and 
posterior  sclerosis  the  lateral  as  well  as  the  posterior  columns  are  in  a 
state  of  sclerosis.  In  some  cases  the  posterior  sclerosis  does  not  reach 
downwards  as  far  as  the  lumbar  region  and  in  these  the  patellar  tendon- 
reactions  are  exaggerated. 

The  diseases  of  the  cerebellum  consist  of  hemorrhage,  softening, 
abscesses,  and  morbid  growths  ;  but  inasmuch  as  their  morbid  anatomy  is 
the  same  as  that  of  other  parts  of  the  brain  it  is  unnecessary  to  consider 
them  further  at  present.  The  tumors  most  frequently  met  with,  especially 
in  young  people,  are  tubercular  growths  and  glioma. 

Morbid  Physiology. — Meniere's  disease  is  caused  by  a  primary  or 
secondary  disease  of  the  semicircular  canals,  and  the  most  consistent 
theory  of  their  functions  is  that  they  are  peripheral  end-organs  of 
afferent  fibres,  Avhose  central  end-organ  is  the  cerebellum.  As  we  have 
seen,  the  cerebellum  is  an  organ  for  adjusting  the  body  to  space  relations, 
and  disease  of  the  peripheral  end-organs  throws  the  whole  of  this 
mechanism  into  disorder,  and  consequently  the  patient  is  unable  to  effect 
those  delicately  coordinated  muscular  contractions  which  are  required 
for  maintaining  various  attitudes  in  space,  and  vertigo  is  the  subjective 
correlative  of  this  objective  fact. 

The  case  of  primary  sclerosis  of  the  columns  of  Goll,  recorded  by 


584  DISORDERS    OF    MOTOR    CO-ORDINATION. 

Pierret  would  seem  to  indicate  that  these  columns  take  some  part  in  the 
function  of  equilibration  in  space.  The  fact  that  these  columns  and  the 
direct  cerebellar  tracts  undergo  an  ascending  sclerosis  proves  that  they 
are  centripetal  conducting  paths,  and  the  fact  that  the  former  terminates 
indirectly  and  the  latter  directly  in  the  cerebellum  appears  to  show  that 
both  tracts  consist  of  cerebello-afferent  fibres.  It  is,  therefore,  likely  that 
the  columns  of  Goll  and  the  direct  cerebellar  tracts  conduct  centripetal 
impulses  to  the  cerebellum,  but  Avhen  sclerosis  of  these  tracts  is  caused 
by  a  transverse  myelitis,  the  symptoms  which  might  be  caused  by  disease 
of  them  are  obscured  by  the  paralysis  which  is  caused -by  arrest  of  con- 
duction through  the  pyramidal  tract. 

In  locomotor  ataxia  the  primary  lesion  is  most  probably  situated  in 
the  posterior  root-zones  of  the  spinal  cord,  and  in  the  homologues  of 
these  tracts  in  the  medulla  oblongata,  pons,  and  crura  cerebri ;  namely, 
the  fasciculus  rotundus,  and  the  ascending  and  descending  roots  of  the 
fifth  nerves.  It  is,  indeed,  supposed  by  Dejerine  that  the  primary 
changes  begin  in  the  peripheral  nerves  and  ascend  through  the  posterior 
roots  to  the  spinal  cord,  and  it  is  at  least  certain  that  the  nerves  of 
special  sense  are  primarily  affected  in  this  peripheral  manner.  But  eyon 
if  the  primary  changes  begin  in  the  peripheral  nerves,  there  can  be  little 
doubt  that  those  portions  of  the  posterior  columns  through  which  the 
afferent  fibres  pass  to  reach  the  posterior  gray  horns  are  involved  in  the 
disease  at  a  very  early  period.  As  the  disease  of  the  posterior  root- 
zones  extends  horizontally  towards  the  posterior  median  fissure,  the 
columns  of  Goll  become  implicated,  and  when  once  the  fibres  of  these 
columns  are  interrupted  in  any  part  of  their  course  the  portions  above 
the  seat  of  the  lesion  undergo  degeneration,  and  in  advanced  cases  these 
columns  are  always  found  in  a  state  of  sclerosis  throughout  their  entire 
length.  The  direct  cerebellar  tracts  are  also  found  in  a  state  of  degenera- 
tion in  long-standing  cases,  and  in  some  cases  the  morbid  process  is 
observed  to  have  extended  to  the  posterior  gray  horns,  the  anterior  gray 
horns,  and  the  lateral  columns.  The  lancinating  pains  may  be  ex- 
plained by  the  irritation  of  the  fibres  of  the  posterior  roots  in  their 
passage  through  the  posterior  columns,  while  the  subsequent  anjiestliesia 
may  be  supposed  to  be  caused  by  destruction  of  these  fibres.  Irritation 
of  the  posterior  gray  horns  causes  the  cutaneous  trophic  changes,  while 
destructive  lesions  of  these  horns  causes  retardation  of  painful  impres- 
sions and  analgesia.  Extension  of  the  lesion  to  the  lateral  columns 
causes  the  paraplegia  which  sometimes  complicates  tabes,  while  impli- 
cation of  the  anterior  gray  horns  causes  the  muscular  atrophy  and 
probably  also  the  arthropathies  of  locomotor  ataxia.  Disease  of  the 
automatic  centres   in  the  lumbar  region  causes  the  vesical  and  sexual 


DISEASES    OF    THE    CEREBELLUM.  535 

disorders.  Parenchymatous  atrophy  of  the  optic  nerves  causes  blindness 
and  white  atrophy  of  the  optic  disks,  and  it  is  pr()bal)le  that  the  disorders 
of  the  other  special  senses,  occasionally  observed,  are  caused  by  degenera- 
tion of  the  respective  nerves.  Absence  of  the  patellar  tendon-reaction 
is  caused  by  disease  of  the  afferent  portion  of  the  reflex  arc  in  its 
passage  through  the  posterior  columns;  while  reflex  pupillary  immo- 
bility is  caused  by  lesion  of  the  fibres  of  the  reflex  loop  which  connect 
the  afferent  fibres  in  the  optic  tract  with  the  efferent  fibres  in  the  third 
nerve.  The  fibres  of  this  reflex  loop  proceed  from  the  anterior  tubercle 
of  the  corpora  quadrigemina  to  the  nucleus  of  the  third  nerve,  and  in 
their  course  they  pass  through  or  near  the  descending  root  of  the  fifth 
nerve,  which  is  as  we  have  seen  the  honiologue  of  the  posterior  root- 
zone  of  the  cord.  The  other  symptoms  which  are  observed  in  the  region 
of  the  cranial  motor  nerves  may  be  explained  by  sclerosis  of  the  fasciculus 
rotundus  and  ascending  root  of  the  fifth  nerve  and  by  an  extension  of 
the  morl>id  process  from  these  bundles  of  nerve  fibres  to  the  nuclei 
themselves.  The  sympathetic  oculo-pupillary  symptoms  are  caused  by 
irritation,  or  more  frequently  by  paralysis,  of  the  fibres  which  proceed 
from  the  dilator  nucleus  through  the  cervical  portion  of  the  cord  to 
emerge  with  the  eighth  cervical  and  first  dorsal  anterior  nerve-roots. 
These  fibres  descend  most  probably  in  the  posterior  root-zones  of  the 
cervical  region  of  the  cord,  and  are  consequently  liable  to  be  implicated 
in  the  disease  at  an  early  period. 

It  now  remains  for  us  to  explain  the  phenomena  of  static  and  dynamic 
ataxia.  Leyden  first  suggested  that  the  ataxia  was  the  result  of  the 
disorders  of  sensibility  which  are  present  in  this  disease,  but  this  theory 
fails  to  account  for  the  well-ascertained  clinical  fact  that,  on  the  one 
hand,  a  slight  degree  of  ataxia  may  be  present  in  the  almost  entire  absence 
of  sensory  disorders,  while,  on  the  other,  there  may  be  an  absence  of 
ataxia  with  a  high  degree  of  anaesthesia.  It  was  suggested  by  Erb  and 
others  that  the  ataxia  was  caused  by  disease  of  motor  or  centrifugal 
paths,  but  this  view  is  not  supported  by  any  well-ascertained  physiological 
or  pathological  facts.  It  seems  probable  that  the  ataxia  is  caused  by 
disease  of  afferent  subconscious  paths.  These  paths  consist  of  afterent 
spinal,  afferent  cerebellar,  and  afferent  subconscious  cerebral  tracts. 
The  posterior  root-zones  themselves  constitute,  most  probably,  afferent 
spinal  paths  for  coordinating  various  reflex  movements,  but  it  is  prob- 
able that  static  ataxia  is  never  present  until  the  columns  of  Goll,  or  the 
direct  cerebellar  tracts  are  implicated  in  the  disease.  It  has  been 
suggested  by  Althaus  that  dynamic  ataxia  is  caused  by  disease  of  the 
afferent  conducting  paths  of  the  basal  cerebral  ganglia,  but  the  tension 
of  the  extensors  of  the  body  which  is  present  in  tabes,  when  the  patient 


536  DISORDERS    OF    ilOTOR    CO  -  0RDI:N^  ATION. 

assumes  the  erect  posture,  would  seem  to  take  an  active  part  in  the  pro- 
duction of  the  ataxic  gait.  This  tension  is  caused  most  likely  by  irrita- 
tion of  cerebello-afferent  paths  and  consequently  irritation  of  these 
paths  is  likely  to  be  one  of  the  main  causes  of  the  ataxic  gait.  When 
the  patient  is  unable  to  maintain  the  erect  posture  the  extensors  of  the 
body  have  lost  their  tension,  and  it  may  then  be  presumed  that  these 
paths  are  more  or  less  destroyed  and  that  cerebellar  paralysis  is  estab- 
lished for  lack  of  communication  with  the  external  world.  All  that 
can  be  said  with  regard  to  the  manner  in  which  disease  of  the  cerebellum 
causes  the  symptoms,  is  implied  in  what  has  already  been  said  respecting 
the  physiology  of  the  organ. 

Treatment. — When  Meniere's  disease  depends  upon  morbid  changes 
in  the  middle  ear  the  patient  should  be  placed  under  the  care  of  the 
aural  surgeon,  and  when  the  local  disease  is  not  accessible  to  treatment 
relief  may  be  obtained  by  rest  in  the  recumbent  posture.  The  adminis- 
tration of  quinine  in  doses  of  from  ten  to  twelve  grains  three  times  a 
day  for  some  days  appears  to  have  produced  great  amelioration  of  the 
symptoms  in  some  cases.  At  first  the  subjective  aural  sounds  caused 
by  the  quinine  are  superadded  to  those  of  the  disease,  and  the  symp- 
toms are  intensified,  but  if  the  quinine  be  omitted  for  eight  or  ten  days 
the  sounds  and  the  vertigo  undergo  notable  diminution.  If  the  quinine 
be  readministered  for  a  period  of  eight  or  ten  days  the  symptoins  arc 
again  aggravated,  to  be  followed  by  a  second  amelioration  on  its  cessation, 
and  after  "a  time  the  attacks  of  vertigo  may  be  completely  arrested. 
Large  doses  of  salicylate  of  sodium  have  also  proven  useful  in  the  treat- 
ment of  the  disease. 

Primary  sclerosis  of  the  columns  of  Goll  requires  to  be  treated  by 
rest  in  the  recumbent  posture  along  with  the  remedies  used  for  other 
forms  of  chronic  myelitis,  while  secondary  sclerosis  of  these  columns 
and  of  the  direct  cerebellar  tracts  does  not  admit  of  treatment  ai)art 
from  the  primary  disease  of  the  cord  which  has  caused  the  sclerosis. 

Locomotor  ataxia  is  so  frequently  preceded  by  syphilitic  infection 
that  in  all  cases  of  the  disease  the  most  careful  investigation  should  be 
instituted  with  the  view  of  discovering  any  indication 'of  the  presence 
of  this  poison.  In  every  case  in  which  a  history  of  syphilis  can  be 
detected,  and  in  all  doubtful  cases,  iodide  of  potassium  in  ten  grain 
doses  three  times  a  day  should  be  given,  and  if  there  are  any  active 
syphilitic  symptoms  present  other  than  the  ataxia,  the  patient  should 
have  a  mercurial  course.  Cases  of  locomotor  ataxia  which  are  comj)li- 
cated  by  spinal  meningitis  are  also  benefited  by  the  administration  of 
iodide  of  potassium.  But  even  when  locomotor  ataxia  is  of  syphilitic 
origin  the  nervous  disease  pursues,  after  a  time,  an  independent  course, 
and  consequently  when  the  patient  has  been  subjected  to  a  thorough 


DISEASES    OF    THE    CEEEBELLUM.  537 

antisyphilitic  treatment,  or  when  the  absence  of  syphilis  has  been 
proved  from  the  first,  other  methods  of  treatment  must  l)e  adopted. 

Of  internal  remedies  nitrate  of  silver,  given  in  doses  of  one-sixth  to 
one-third  of  a  grain  three  times  a  day  is  probably  the  most  generally 
useful.  It  may  be  continued  for  three  weeks  at  a  time,  and  then  after 
an  interruption  of  two  Aveeks  its  use  may  be  resumed  for  another  three 
weeks.  The  use  of  the  remedy  may  be  continued  in  this  way  with 
repeated  interruptions  for  many  months  without  producing  deleterious 
effects.  If  the  skin  shows  the  slightest  discoloration,  the  medicine 
must,  of  course,  be  interrupted  for  a  longer  period.  Belladonna,  arsenic, 
chloride  of  gold  and  sodium,  and  chloride  of  barium  have  also  been 
employed  in  the  treatment  of  tabes,  but  not  apparently  with  much 
success.  The  administration  of  ergot  is  sometimes  beneficial,  but  it 
ought  to  be  given  with  caution,  as  diseased  rye  is  known  to  cause  scle- 
rosis of  the  posterior  columns  of  the  cord.  Phosphorus,  either  alone  or 
with  cod-liver  oil,  has  sometimes  been  found  useful.  Strychnine  is 
always  useless  and  dangerous. 

Thermal  baths  may  be  soothing  to  the  patient  during  severe  attacks 
of  lancinating  pains,  but  they  do  not  appear  to  exercise  a  favorable 
influence  over  the  course  of  the  disease. 

Saline  thermal  baths  appear  to  act  favorably,  and  those  of  Rheims 
and  Nanheim  have  been  favorably  reported  upon.  Sulphur,  chaly- 
beate, and  mud  baths  have  been  employed,  but  it  is  doubtful  whether 
they  do  any  good  except  by  improving  the  general  health  of  the  patient. 

Hydr other a'peutics,  as  carried  out  in  well-conducted  hydropathic 
establishments,  is  a  very  useful  adjunct  in  the  treatment  of  many  cases 
of  tabes.  The  institution  should  be  situated  in  an  elevated  region,  so 
that  the  patient  may  have  the  advantage  of  a  pure  mountain  air.  This 
treatment  answers  best  in  the  summer  season.  The  wet  pack  should 
be  used  with  caution,  beginning  with  a  temperature  of  88°  F.  and 
going  down  to  77°  F.  Wet  rubbings  are  useful,  beginning  Avith  a 
temperature  of  77°  F.  and  going  down  to  65°  F. 

Electrical  treatment  exercises  a  favorable  influence  on  the  progress 
of  the  disease.  The  constant  current  is  usually  employed,  and  both 
electrodes  should  be  placed  on  the  vertebral  column — one  in  the  lumbar 
region  and  the  other  at  the  nucha.  One  pole,  say  the  lower,  should  be 
fixed  and  the  other  slowly  moved  along  the  back  so  as  to  come  in 
contact  with  every  part  of  the  vertebral  column ;  then  the  upper  pole 
should  be  fixed,  and  the  lower  one  slowly  moved  along  tlie  back.  The 
direction  of  the  current  is  of  no  consequence.  The  current  should  be 
applied  daily,  but  each  sitting  should  not  be  for  more  than  from  three 
to  six  minutes'  duration.     Strong  currents  should  be  avoided,  especi- 


538  DISOEDERS    OF    MOTOR    CO  -  O  R  DIN  ATIOX  . 

ally  in  irritable  persons  with  severe  pains.  The  application  of  the 
fai-adic  brush  to  the  surface  of  the  body  is  useful  when  there  is  marked 
anaesthesia.  The  positive  pole  should  be  placed  on  the  sternum,  and 
the  negative  pole,  with  the  brush,  drawn  repeatedly  along  the  vertebral 
column  and  then  along  the  extremities. 

Favorable  results  have  been  obtained  by  Dr.  Mortimer  Granville  by 
means  of  nerve  vibration,  I  have  given  a  trial  to  this  treatment  in 
some  cases,  and  found  it  very  grateful  to  the  patients,  although  I  cannot 
say  that  it  appeared  to  be  of  much  use  in  other  respects. 

Nerve-stretching  has  been  used  as  a  means  of  treatment  in  locomotor 
ataxia.  It  is  possible  that  the  lancinating  pains  may  be  rendered  more 
tolerable  by  this  treatment,  but  after  witnessing  the  effects  of  the  treat- 
ment in  a  few  cases,  I  am  not  disposed  to  hazard  further  trial  of  it 
myself  or  to  recommend  it  to  others. 

The  treatment  of  tabes  b}"  complete  rest  in  the  recumbent  position, 
which  was  first  reconun ended  by  Dr.  S.  Weir  Mitchell,  appears  to  be 
one  of  the  most  successful  methods  which  can  be  adopted,  but  it  is  only 
in  exceptional  cases  that  patients  can  be  induced  to  lie  in  bed  for  any 
considerable  period  of  time  so  long  as  they  are  able  to  move  about  at  all. 

Amongst  various  remedies  which  have  been  used  against  the  lancinat- 
ing pains  may  be  mentioned  sinapisms,  blisters,  Avarmth,  Priessnitz's  cold- 
water  compresses,  belladonna  plasters,  chloroform  and  other  liniments, 
faradization  or  galvanization  of  the  hypeniesthetic  spots  (stabile  anode), 
subcutaneous  injections  of  morphine,  and  large  doses  of  the  bromide  of 
potassium,  or  of  the  hydrobromate  of  quinine,  and  large  doses  of  iodide 
of  potassium  when  the  symptoms  indicate  the  presence  of  meningitis. 
One  patient  told  me  that  he  found  most  relief  from  the  lancinating 
pains  by  hot  ironing  the  painful  joints.  AVhen  antesthesia  is  present 
cutaneous  faradization  may  be  employed  with  benefit. 

In  vesical  weakness  faradization  of  the  bladder,  either  with  or  with- 
out the  aid  of  the  bladder  electrode,  may  be  usefully  employed.  Cystitis 
must  be  treated  in  the  same  way  as  in  chronic  myelitis. 

Constipation  must  be  combated  by  mild  aperients,  enemata,  and 
regulation  of  diet,  or  by  fiiradization. 

The  treatment  of  the  diseases  of  the  cerebellum  must  depend  upon 
the  nature  of  the  lesion.  In  hemorrhage  the  treatment  is  the  same  as 
for  cerebral  hemorrhage,  and  it  seems  to  me  that  there  may  be  a  possi- 
bility of  our  being  able,  in  some  cases,  to  evacuate  the  pus  through  the 
temporal  bone.  In  tubercular  growths,  glioma,  and  other  tumors,  little 
can  be  done  beyond  palliative  treatment,  unless,  indeed,  the  growth  be 
of  syphilitic  origin,  when  an  energetic  antisyphilitic  treatment  may 
procure  partial  or,  on  rare  occasions,  more  or  less  complete  recovery. 


CHAPTER    X. 

VASCULAR  DISEASES  OF  THE  SPINAL  CORD. 

I.  ANEMIA,  THKOMBOSIS,  AND   EMBOLISM    OF    THE   SPINAL 
CORD    (MYELOMALACIA,  VASCULAR   SPINAL   SCLEROSIS). 

Etiology. — The  predisposing  causes  of  spinal  antemia  are  congenital 
narrowness  of  the  calibre  of  the  vessels,  weakness  of  the  heart,  and 
undue  excitability  of  the  vaso-motor  nerves  giving  rise  to  vascular 
spasm.  Anaemia  of  the  cord  is  often  only  an  expression  of  general 
anjBmia  caused  by  hemorrhages,  and  dyscrasic  conditions  like  chlorosis, 
pernicious  anaemia,  and  other  cachectic  diseases.  Spinal  ansemia  occurs 
much  more  frequently  in  the  female  than  in  the  male  sex.  In  some 
cases  the  anaemia  is  caused  by  extensive  atheromatous  changes  of  the 
spinal  bloodvessels,  or  by  the  arterio-capillary  fibrosis  which  accompanies 
chronic  interstitial  nephritis.  When  the  vessels  are  extensively  changed 
by  atheroma,  thrombosis  may  take  place  to  such  an  extent  that  softening 
occurs,  a  condition  Avhich  has  been  named  myelomalacia,  but  arterio- 
capillary  fibrosis  is  more  likely  to  give  rise  to  sclerosis  of  the  walls  of 
the  vessels  and  of  the  tissues  in  their  immediate  vicinity,  a  condition 
which  may  be  named  diffused  vascular  sclerosis.  The  anastomosis  of 
the  spinal  vessels  is  so  free  that  embolism  of  them  is  not  likely  to  give 
rise  to  extensive  softening,  but  the  multiple  embolism  which  occurs  in 
cases  of  chorea  sometimes  gives  rise  to  small  spots  of  necrotic  softening 
in  the  cord.  The  greatest  degree  of  ansemia  of  the  spinal  cord  is 
caused  by  compression,  thrombosis,  or  embolism  of  the  abdominal  aorta 
above  the  point  of  origin  of  the  lumbar  arteries. 

Symptoms. — When  the  abdominal  aorta  is  suddenly  obliterated  by  a 
large  embolus  the  lower  extremities  become  quickly  paralyzed,  and 
every  form  of  sensibility  is  lost  in  them ;  the  reflex  excitability  and  the 
tendon-reactions  are  also  abolished,  and  the  bladder  and  rectum  are 
paralyzed.  If  the  obliteration  of  the  aorta  takes  place  more  slowly 
the  symptoms  develop  gradually  and  are  less  severe;  they  consist  of 
a  feeling  of  numbness  in  the  lower  extremities,  which  also  feel  weak 
and  easily  tired  on  slight  exertion.  Nothing  is  known  of  the  symptoms 
caused  by  ischsemia  of  the  cervical  region  of  the  spinal  cord.  The 
ischaemia  caused  by  vaso-motor  spasm    is  characterized  by  the  same 


540  VASCULAR    DISEASES    OF    THE    SPINAL    CORD. 

kind  of  symptoms  as  those  resulting  from  aortic  obstruction,  although 
they  are  much  less  severe  in  the  former  than  in  the  latter.  In  this 
form  of  anaemia  some  source  of  peripheral  irritation  can  usually  be 
discovered,  and  the  paralytic  symptoms  generally  disappear  if  the 
source  of  irritation  be  removed. 

In  the  spinal  ansemia  which  results  from  general  causes  the  most 
constant  symptoms  are  motor  weakness,  first  in  the  lower  and  subse- 
quently in  the  upper  extremities,  and  tremor  on  the  slightest  exertion, 
and  in  some  cases  complete  paralysis  may  be  developed.  The  sensory 
disorders  consist  of  various  parsesthesije,  pain,  hyperesthesia,  and,  on 
rare  occasions,  a  slight  degree  of  amvsthesia.  The  cutaneous  reflexes 
and  tendon-reactions  are  often  exaggerated,  and  the  sphincters  are  not, 
as  a  rule,  affected.  It  is  said  that  the  symptoms  improve  on  lying 
doAvn,  and  on  the  contrary  are  made  worse  when  the  patient  assumes 
the  erect  posture.  The  spinal  symptoms  are  associated  with  the  usual 
symptoms  of  general  anaemia  or  of  chloi'osis. 

In  myelomalacia  the  symptoms  are  very  obscure.  The  patient  first 
complains  of  numbness  and  feebleness  of  the  lower  extremities,  and 
these  symptoms  gradually  increase  in  intensity  until  ultimately  anaes- 
thesia and  complete  paralysis  of  the  lower  extremities  are  fully  estab- 
lished. The  cutaneous  reflexes  are  also  diminished  and  finally  abol- 
ished in  the  loAver  extremities,  but  the  patellar  tendon-reactions  may 
be  retained  for  a  long  time.  As  the  disease  advances  the  spliincters  of 
the  bladder  and  rectum  become  gradually  paralyzed,  and  ultimately  the 
patient  dies  from  bedsores,  marasnms,  and  pyaemia.  Hypemesthesia, 
spasms,  or  increase  of  the  cutaneous  reflexes,  are  said  to  be  absent 
throughout  the  course  of  the  disease. 

In  diffused  vascular  sclerosis  the  symptoms  pursue  a  chronic  course, 
and  are  for  a  long  time  like  those  of  a  primary  lateral  sclerosis,  with 
an  admixture  of  indefinite  sensory  disorders.  The  sphincters  are  not 
affected  until  a  late  period  of  the  disease. 


II.  HYPEK.EMIA  AND  HEMORRHAGE  OF  THE  SPIXAL  CORD. 

1.  Spinal  Hyper/EMIa. 

Etiology. — Hyperaemia  of  the  cord  is  produced  by  excessive  func- 
tional activity,  such  as  occurs  in  severe  exertion  or  violent  sexual  ex- 
citement. Congestion  being  present  in  the  early  stages  of  inflamma- 
tion, all  the  causes  of  myelitis  likewise  give  rise  to  hyperaemia.  It 
may  also  be  caused  by  various  toxic  agents,  such  as  strychnine,  carbonic 


HYPER.EMIA   AND   HEMORRHAGE   OF    SPINAL   CORD.      541 

oxide,  and  alcoholic  excess.  Passive  hypersemia-  is  caused  by  those 
conditions  which  flivor  general  venous  congestion,  such  as  diseases  of 
the  heart  and  lungs,  or  convulsive  diseases  like  tetanus,  epilepsy,  and 
eclampsia. 

Symptoms. — The  most  prominent  symptoms  of  spinal  hypersemia 
are  pains  in  the  loins,  and  along  the  spine,  of  a  dull  oppressive  char- 
acter, and  which  are  not  increased  on  pressure.  The  patient  com- 
plains of  tingling,  formication,  and  tearing  pains  in  the  lower  extremi- 
ties, and  a  slight  degree  of  hyper?esthesia  of  the  skin,  a  girdle  sensation, 
and  a  moderate  increase  of  reflex  activity  may  be  present.  The  motor 
symptoms  consist  of  transitory  jerking  of  the  muscles  and  trembling  of 
the  limbs,  and  Rosenthal  says  that  the  electrical  excitability  is  increased. 
In  severer  cases  the  patient  complains  of  numbness  in  the  lower  ex- 
tremities, the  limbs  feel  heavy  and  feeble,  and  the  patient  feels  tired  on 
slight  exertion,  but  complete  paraplegia  probably  never  occurs.  The 
sensory  and  motor  disorders  may  occasionally  implicate  the  upper 
extremities,  and  in  those  cases  respiration  is  said  to  have  been  disturbed. 
The  symptoms  are  said  by  Brown-Sequard  to  be  aggravated  by  lying 
on  the  back  with  the  head  and  legs  raised,  while  they  are  relieved  by 
lying  on  the  ftice,  standing  or  walking,  and  the  patients  are  said  to  feel 
worse  before  getting  up  in  the  morning.  If  the  congestion  is  sufficiently 
intense  to  give  rise  to  serous  effusion  the  patients  feel  better  in  the 
horizontal  position.  There  is  no  fever,  and  the  pulse  may  be  either 
quick  or  slow  if  the  hypera^mia  extend  to  the  spinal  centres  of  cardiac 
innervation.  Passive  must  be  distinguished  from  active  congestion  by 
the  presence  or  absence  of  general  venous  congestion.  Spinal  hypere- 
mia ends  in  recovery  unless  the  case  prove  fatal  from  a  cardiac  or  some 
other  complication. 

2.  Spinal  Apoplexy  (H.ematomyelia). 

Etiology. — Spinal  apoplexy  is  more  common  in  youth  and  middle 
age  than  in  old  age,  attaining  its  greatest  frequency  between  twenty 
and  thirty-five  years  of  age.  Men  are  more  subject  to  the  disease  than 
women  in  the  proportion  of  about  four  to  one.  Amongst  the  exciting 
causes  are  traumatic  injuries,  suppression  of  accustomed  discharges, 
active  congestion  of  the  cord,  and  the  presence  of  a  rapidly  growing 
tumors  like  glioma. 

Symptoms. — The  disease  may  be  preceded  by  obscure  premonitory 
symptoms  like  those  of  congestion  of  the  cord,  which  may  last  from  a 
few  hours  to  several  days,  but  even  in  those   cases  the  onset  of  the 


542  VASCULAR    DISEASES    OF    THE    SPINAL    CORD. 

characteristic  symptoms  is  always  sudden,  and  complete  paraplegia 
develops  in  the  course  of  a  few  minutes  or  at  most  an  hour.  During 
the  development  of  the  paralysis  the  patient  often  complains  of  a  violent 
pain,  which  is  either  localized  at  a  particular  spot,  extends  along  the 
spinal  column,  or  shoots  in  the  form  of  a  girdle  round  the  l)ody  ;  but 
when  the  paralysis  has  become  complete  the  pain  usually  disappears, 
although  the  spinous  processes  of  the  vertebrae  over  the  seat  of  the  lesion 
may  remain  tender  to  pressure,  or  to  the  cathode  of  a  galvanic  current, 
for  a  considerable  time.  When  the  lower  cervical  region  is  implicated 
the  paraplegia  extends  to  the  upper  extremities,  the  respiratory  muscles 
are  paralyzed,  and  the  breathing  is  diaphragmatic.  The  paralyzed 
muscles  are  at  first  flaccid,  and  the  reflexes  and  tendon-reactions  are 
absent  in  the  lower  extremities,  from  the  shock,  even  in  the  cases  in 
Avhich  the  lesion  is  situated  high  up. 

In  the  early  stage  there  is  more  or  less  complete  aniTesthesia  of  every 
form  of  sensibility,  having  in  most  cases  the  same  distribution  as  the 
motor  paralysis,  but  when  the  lesion  is  unilateral  there  may  be  hyper- 
sesthesia  of  one  of  the  lower  extremities  and  anaesthesia  of  the  other 
even  although  both  limbs  may  be  paralyzed.  Ketention  of  urine  may 
be  present  from  the  first  from  interference  with  the  conducting  paths, 
or  the  shock  may  give  rise  to  a  transient  incontinence,  but  permanent 
incontinence  of  urine  and  feces  only  occurs  when  the  automatic  centres 
of  the  bladder  and  rectum  are  invaded  by  the  hemorrhage  or  are 
secondarily  implicated  by  the  inflannnatory  reaction.  Priapism  is  a 
frequent  symptom  during  the  first  few  days,  and  the  temperatui-e  of  the 
paralyzed  extremities  may  be  raised  from  0.2°  to  2°  C.  above  that  of 
the  axilla.  In  the  course  of  a  few  days  the  symptoms  of  secondary 
myelitis  may  be  superadded  to  those  caused  by  the  primary  lesion,  and 
then  the  patient  may  suff"er  from  pains  of  various  forms,  and  twitching 
movements  and  jerkings  of  the  extremities.  If  the  myelitis  extends 
downwards  so  as  to  reach  the  level  of  the  upper  lumbar  region  of  the 
cord  the  sphincters  become  paralyzed,  cystitis  and  bedsores  appear,  and 
the  patient  dies  from  septic  fever  ;  and  if  it  ascend  to  the  upper  cervical 
region  the  patient  dies  from  asphyxia. 

If  the  patient  survive  the  stage  of  secondary  myelitis  signs  of  im- 
provement begin  to  show  themselves.  In  those  cases  in  which  there  is 
hypenesthesia  of  one  lower  extremity  and  anaesthesia  of  the  other,  the 
anaesthetic  extremity  gradually  regains  its  motor  power  and  it  may 
ultimately  be  almost  completely  restored,  but  the  hyperaesthetic  extremity 
becomes  the  seat  of  a  permanent  spasmodic  paralysis  with  exaggerated 
reflexes  and  tendon-reactions.  If  the  upper  extremities  are  paralyzed 
the  one  on   the  anaesthetic  side  may  also  recover,  while  the  paralyzed 


HYPEK.EMIA    AND   HEMORRHAGE   OF   SPINAL   CORD.       543 

muscles  of  the  opposite  upper  extremity  remain  permanently  paralyzed 
and  undergo  atrophy,  being  innervated  from  the  level  of  the  lesion. 

The  sensory  disorders  also  undergo  some  improvement.  The  hyper- 
8esthesia  may  gradually  disappear  from  the  lower  extremity  which  is 
permanently  paralyzed,  but  the  anaesthesia  often  remains  more  or  less 
permanent  in  the  lower  extremity  which  has  recovered  motor  poAver, 
and  it  also  extends  over  the  half  of  the  body  on  that  side  up  to  the  area 
of  distribution  of  the  sensory  nerves  derived  from  the  upper  limit  of  the 
lesion.  On  the  paralyzed  side,  although  the  sensibility  has  become 
normal  below  the  level  of  the  lesion,  yet  a  band  of  anaesthesia  extends 
round  the  half  of  the  body  corresponding  to  the  vertical  extent  of  the 
lesion. 

The  immediate  and  permanent  symptoms  will,  of  course,  vary  accord- 
ing to  the  extent  and  situation  of  hemorrhage,  and  in  cases  which  make 
a  partial  recovery  the  lesion  is  generally  limited  to  one-half  of  the  cord. 
In  small  hemorrhages  it  may  not  be  possible  to  make  a  certain  diagnosis 
of  the  nature  of  the  lesion.  When,  for  example,  the  hemorrhage  remains 
limited  to  the  anterior  eornua  the  chief  symptom  will  be  the  sudden 
occurrence  of  an  atrophic  paralysis  and  the  case  should  be  regarded  as 
very  acute  anterior  poliomyelitis. 

If  the  lumbar  region  of  the  cord  be  the  seat  of  the  hemorrhage  the 
symptoms  of  paralysis  and  anaesthesia  are  limited  to  the  lower  extremities ; 
the  muscles  of  the  lower  extremities  undergo  a  diffused  atrophy  and 
manifest  the  reaction  of  degeneration  ;  the  patellar  tendon-reactions  are 
lost,  but  the  reflex  of  the  sole  may  still  be  retained ;  the  bladder  and 
rectum  are  paralyzed  ;  cystitis  and  bedsores  appear  at  an  early  period, 
and  the  patient  dies  from  septic  fever.  If  the  lesion  is,  however,  very 
limited  and  situated  below  the  level  of  the  automatic  centres  of  the 
bladder  and  rectum  gradual  recovery  may  take  place,  the  paralysis  of 
the  sphincters  which  was  present  at  first  disappears,  the  sensory  dis- 
orders improve,  but  the  muscles  of  the  lower  extremity  on  the  side  of 
the  lesion  undergo  a  diff'used  atrophy,  and  one  or  more  groups  may 
remain  permanently  paralyzed,  but  the  other  lower  extremity  often  gives 
signs  of  a  slight  degree  of  spasmodic  paralysis. 

If  the  dorsal  region  be  the  seat  of  the  hemorrhage  the  patient  recovers, 
unless  a  secondary  myelitis  supervene  and  prove  fatal.  The  permanent 
symptoms  will  be  a  spasmodic  paralysis  of  the  lower  extremity  on  the 
side  of  the  lesion  and  an  atrophic  paralysis  of  the  dorsal,  abdominal,  or 
intercostal  muscles  supplied  from  the  level  of  the  lesion.  There  will  be 
anaesthesia  of  the  lower  extremity  and  of  the  half  of  the  body  on  the 
opposite  side  to  that  of  the  inner  paralysis,  and  a  band  of  amijsthesia 


64:4:  VASGULAE    DISEASES    OF    THE    SPIRAL    COED. 

surrounding  the  body  on  the  side  of  the  lesion  and  corresponding  to  the 
vertical  extent  of  the  lesion. 

If  the  lower  cervical  or  upper  dorsal  regions  are  the  seat  of  the 
hemorrhage  the  permanent  symptoms  will  be  a  spasmodic  paralysis  of 
the  lower  extremity  and  an  atrophic  paralysis  of  groups  of  muscles  of 
the  upper  extremity  and  of  the  upper  intercostal  muscles  on  the  side  of 
the  lesion,  hemiansesthesia  on  the  opposite  side  of  all  points  below  the 
level  of  the  upper  limit  of  the  lesion,  and  on  the  side  of  the  lesion  a 
band  of  anaesthesia  encircling  half  the  body  and  an  area  of  aniTesthesia 
of  variable  distribution  in  the  upper  extremity.  In  addition  to  the 
motor  and  sensory  disorders,  oculo-pupillary  phenomena  are  found  on 


the  side  of  the  lesion.  In  a  case  of  spinal  hemorrhage  which  has  been 
under  my  observation  for  many  years  the  permanent  symptoms  are  a 
spasmodic  paralysis  of  the  right  lower  extremity  and  an  atrophic  paral- 
ysis of  the  intercostal  muscles  from  the  ninth  upwards,  and  of  the  small 
muscles  of  the  hand  and  the  flexors  of  the  fingers  and  wrist.  The  hand 
assumes  the  well-known  claw-form  met  with  in  cervical  pachymeningitis 


IIYPER^EMIA   AND   HEMORRHAGE   OF   SPINAL   CORD.      545 

when  the  lesion  is  situated  on  a  level  with  the  eighth  cervical  and  first 
dorsal  nerves.  On  the  left  side,  the  lower  extremity  and  the  half  of  the 
body  up  to  the  level  of  the  clavicle  are  almost  completely  anaesthetic,  the 
skin  of  the  right  lower  extremity  and  of  the  half  of  the  body  up  to  the 
level  of  the  tenth  rib,  which  was  at  first  hypenesthetic,  is  now  normal, 
but  above  the  tenth  rib  a  band  of  anaesthesia  encircles  half  the  body  up 
to  the  level  of  the  clavicle,  while  the  anaesthetic  area  extends  down  the 
inner  aspect  of  the  arm  and  forearm,  the  ulnar  half  of  the  palm  and 
back  of  the  hand  and  two  and  a  half  fingers  (Fig.  170).  The  oculo- 
pupillary  symptoms  are  well  marked  in  the  right  eye. 

If  the  lesion  extends  further  up  in  the  cervical  region  other  groups 
of  muscles  will  be  paralyzed  in  the  upper  extremity  and  the  area  of 
distribution  of  the  anaesthesia  will  also  be  different  from  that  of  the  case 
just  described.  If  the  hemorrhage  occur  above  the  origin  of  the  phrenic 
nerves,  rapid  death  by  asphyxia  is  inevitable. 

Morbid  Physiology. — Ancemia  of  the  spinal  cord  had  been  experi- 
mentally produced  in  animals  by  Stenon  as  far  back  as  1667,  and  since 
that  time  by  various  other  physiologists,  but  the  most  complete  and 
conclusive  experiments  of  this  kind  were  performed  by  Kussmaul  and 
Tenner.  These  experimentalists  first  tied  the  subclavian  arteries,  and 
so  arrested  the  circulation  through  the  vertebral  arteries.  Compression 
upon  the  descending  portion  of  the  arch  of  the  aorta  now  caused  more  or 
less  complete  arrest  of  the  circulation  in  the  cord,  and  after  a  minute  and 
a  half  the  animals  operated  upon  became  paralyzed  in  their  posterior 
extremities,  but  the  paralysis  soon  extended  upwards,  and  death  re- 
sulted from  paralysis  of  respiration.  Inert  powders  have  been  injected 
into  the  aorta  of  animals  by  Panum  and  A\dpian,  with  the  result  of 
obliterating  a  large  number  of  the  small  bloodvessels  of  the  abdominal 
organs  and  of  the  lower  part  of  the  si»inal  cord.  The  operation  Avas 
almost  immediately  followed  by  paralysis  of  both  sensation  and  motion 
of  the  posterior  extremities,  and  after  death  foci  of  softening  were 
found  in  the  spinal  cord.  These  experiments  show  that  arrest  of  the 
circulation  through  the  cord,  either  by  occlusion  of  the  large  vessels 
from  which  the  cord  derives  its  arterial  supply,  or  of  a  large  number  of 
the  vessels  of  the  cord  itself,  is  followed  by  a  cessation  of  the  spinal 
functions. 

Hypercemia  of  the  spinal  cord  gives  rise  at  first  to  slight  irritative 
sensory  and  motor  phenomena,  but  these  soon  give  place  to  depressive 
symptoms.  The  primary  irritative  symptoms  are  caused  by  the  free 
supply  of  nourishment  conveyed  to  the  cord  by  the  well-filled  vessels, 
but  as  the  vessels  become  greatly  distended  the  nervous  tissues  are  com- 

35 


54:6  VASCULAK    DISEASES    OF    THE    SPINAL    CORD. 

pressed,  the  material  exchanges  are  in  great  part  arrested,  and  the  irri- 
tation gives  place  to  depressive  s^^mptoms. 

Hemorrhage  of  the  spinal  cord  is  said  by  Hayem  and  Charcot  to 
be  always  a  secondary  result  of  hyperacute  myelitis  or  of  some  other 
disease  of  the  spinal  cord.  It  is  probable  that  hemorrhagic  infiltration 
is  always  the  result  of  a  very  acute  central  myelitis,  and  a  hemorrhagic 
clot  sometimes  occurs  as  a  grave  and  generally  fiital  complication  of  a 
chronic  spinal  disease  like  progressive  muscular  atrophy.  In  other  cases, 
however,  the  sudden  onset  of  the  disease  and  the  absence  of  all  irritative 
symptoms  as  well  as  of  power,  seem  to  indicate  that  the  henmrrhage 
is  primary,  and  that  any  evidence  of  myelitis  which  may  be  present  in 
the  cord  after  death  is  caused  by  a  secondary  myelitis.  The  character 
of  the  symptoms  will  depend  upon  the  extent  and  localization  of  the 
hemorrhage,  the  degi'ee  of  secondary  myelitis,  and  the  tracts  of  the 
cord  which  have  been  destroyed. 

Treatment. — In  the  treatment  of  spinal  ancemia  the  causes  must  be 
removed  by  a  tonic  and  stimulating  treatment.  In  aggravated  cases 
the  patient  should  be  laid  on  his  back  and  his  legs  raised,  and  this 
position  should  be  maintained  during  the  night  and  for  a  considerable 
portion  of  the  day.  Strychnine  may  be  administered  in  spinal  antijmia, 
and  the  constant  current  should  be  applied  daily  to  the  vertebral 
column,  while  the  faradic  current  may  be  applied  to  the  paralyzed 
muscles  if  the  reflexes  are  not  in  excess.  Chapman's  spinal  bag,  filled 
with  hot  water,  or  hot  sand-bags,  may  be  applied  along  the  back.  The 
diet  should  be  generous  and  moderately  stimulating. 

In  spinal  hyperceinia  leeches  may  be  ap}»liod  along  the  spine,  especi- 
ally when  the  affection  is  caused  by  the  suppression  of  accustomed  dis- 
charges. A  saline  purgative  may  be  of  use  by  unloading  the  vessels 
and  lowering  the  arterial  tension.  Ergotine  and  belladonna  arc  the 
favorite  internal  remedies.  The  patient  should  be  directed  to  lie  on 
his  side,  or  in  the  prone  position,  and  Chapman's  ice-bag  may  be 
applied  to  the  spine.  The  cold  effusion,  douches,  cold  packing,  and 
sea  baths  may  take  the  place  of  the  ice-bag.  The  diet  siiould  be  plain, 
nourishing,  and  unstimulating,  and  everything  which  might  increase  the 
hypereemia,  such  as  sexual  and  alcoholic  indulgence,  must  be  avoided. 

Spinal  hemorrh<(;/e  mii^t  be  treated  ^at  first  like  spinal  hyperaemia, 
and  after  a  time  like  an  ordinary  case  of  myelitis. 


CHAPTER     XI. 

MYELITIS. 

The  forms  of  myelitis  which  affect  exclusively  the  embryological 
systems  of  the  spinal  cord  have  already  been  considered,  and  conse- 
quently there  remain  for  discussion  only  those  kinds  in  which  the  gray 
and  white  substances  are  indiscriminately  attacked,  and  in  which  the 
symptoms  of  atrophic  and  spasmodic  paralysis,  along  with  various  dis- 
orders of  sensation  and  of  the  functions  of  the  bladder  and  rectum,  are 
associated  in  the  same  case.  When  inflammation  affects  several  of  the 
embryological  systems  of  the  spinal  cord  it  may  be  named  diffused  or 
indiscriminate  myelitis. 

Etiology. — Many  cases  of  myelitis  begin  in  the  absence  of  any  rec- 
ognizable exciting  or  predisposing  cause.  Males  appear,  to  be  more 
liable  to  myelitis  than  females,  and  the  majority  of  cases  occur  between 
ten  and  thirty  years.  Sexual  excess  and  severe  bodily  exertion  act  as 
predisposing  causes. 

The  most  usual  exciting  causes  are  wounds,  fractures,  and  contusions 
of  the  vertebral  column,  extension  of  inflammation  to  the  cord  from 
disease  of  the  membranes  or  vertebrfB,  and  exposure  to  cold  when  the 
body  is  overheated.  jNIyelitis  may  also  be  caused  by  an  ascending 
neuritis  set  uj)  by  irritative  lesion  of  the  joints  and  internal  organs, 
especially  the  genito-urinary  organs.  It  may  also  occur  as  a  complica- 
tion or  sequel  of  the  acute  specific  fevers,  acute  rheumatism,  and  severe 
puerperal  diseases,  and  a  very  acute  form  of  myelitis  is  liable  to  occur 
in  syphilitic  subjects. 

Any  condition,  indeed,  which  narrows  the  spinal  canal  and  leads  to 
compression  of  the  cord  may  become  a  cause  of  myelitis.  Of  these 
causes  caries  of  the  vertebrae  is  the  most  frequent  and  important.  The 
cord  may  be  subjected  to  compression  by  the  bodies  of  diseased  verte- 
brae, displaced  fragments  of  bone,  or  protruding  intervertebral  carti- 
lages. More  frequently,  however,  the  cause  of  compression  is  to  be 
found  in  the  accumulation  of  inflammatory  products  around  the  mem- 
branes, or  secondary  inflammatory  thickening  of  the  dura  mater  itself. 
Amongst  other  diseases  of  the  vertebrae  which  occasionally  cause  com- 
pression of  the  cord  may  be  mentioned  exostosis,  syphilitic  new  forma- 
tions, dry  arthritis  of  the  vertebrge,  and  thickening  of  the  odontoid 


548  MYELITIS. 

process  of  the  axis.  External  tumors  of  all  kinds,  such  as  carcinomata, 
sarcomata,  and  echinococci  may,  by  effecting  an  entrance  into  the  ver- 
tebral canal,  occasion  more  or  less  sudden  compression  of  the  cord,  or 
even  give  rise  to  a  secondary  myelitis  in  the  absence  of  compression. 
Intramedullary,  meningeal,  and  perimeningeal  tumors  of  all  kinds  give 
rise  to  myelitis  by  compression,  and  of  these  it  is  important  to  remember 
that  syphilitic  deposit  is  the  most  frequent. 

Symptoms. — The  spinal  phenomena,  in  acute  cases,  are  often  pre- 
ceded by  premonitory  symptoms  consisting  of  general  malaise,  slight 
pyrexia,  chilliness,  headache,  general  depression,  loss  of  a])petite,  and 
aching  of  the  limbs.  The  spinal  symptoms  generally  manifest  them- 
selves by  sensory  disturbances  consisting  of  girdle  pains  ;  numbness, 
and  various  other  paraesthesije,  along  with  shooting,  burning,  and  other 
sensations  in  the  limbs  :  by  pain  in  the  back  over  the  vertebral  column, 
which  is  accompanied  by  tenderness  on  pressure  of  the  spinous  pro- 
cesses, and  by  superficial  sensitiveness  that  can  be  elicited  by  passing  a 
hot  sponge  or  the  cathode  of  the  galvanic  current  over  the  part.  Patients 
complain  at  times  of  painful,  dragging  sensations  in  tlie  l)laddcr  and 
rectum,  gastralgic  attacks,  and  neuralgic  pains  in  other  viscera.  As  the 
disease  advances  the  parjesthesiie  and  pains  give  place  to  an;estliesia, 
Avhich  may  be  partial  or  complete,  although  even  when  sensation  is 
wholly  lost  to  objective  examination  the  patient  may  complain  of  severe 
pains  in  the  i)art — anceHthenia  dolorosa.  In  most  severe  cases  the 
amesthetic  lower  ])art  of  the  body  is  se])arated  from  the  normal  skin  by 
a  pretty  sharply  defined  line. 

The  motor  symptoms  consist  at  first  of  twitchings  of  individual 
muscles  or  of  entire  extremities,  and  occasionally  the  spasm  may  increase 
to  a  condition  of  tetanic  rigidity.  But  the  symptoms  of  motor  irrita- 
tion soon  give  place  to  paralysis,  and  loss  of  motor  power  is  sometimes 
developed  Avith  so  much  rapidity  that  we  speak  of  apoplectiform  myelitis. 
When  paralysis  is  rapidly  developed  the  muscles  are  perfectly  flaccid, 
and  when  the  limbs  are  raised  they  fall  like  inert  and  lifeless  masses. 
If  the  patient  survive,  symptoms  of  motor  irritation  may  reappear  in 
the  affected  limbs,  consisting  of  spontaneous  twitchings  of  the  paralyzed 
muscles,  Avhich  are  generally  accompanied  by  severe  shooting  pains. 
The  muscles  now  become  tense,  and  the  tension  is  increased  by  passive 
movements  of  the  limbs,  while  contractures  become  established  which 
fix  the  lower  extremities  generally  in  positions  of  extension  and  only 
occasionally  in  flexion.  The  most  common  forms  of  paralysis  are  para- 
plegia and  hemiparaplegia,  while  complete  paralysis  of  all  four  ex- 
tremities occurs  occasionally. 

The  reflex  excitability  and  tendon-reactions  vary  according  to  the 


SYMPTOMS.  549 

seat  of  the  disease.  When  the  disease  involves  the  lumbar  enlargement 
l)otli  the  reflex  of  the  sole  and  the  patellar  tendon-reaction  are  abolished  ; 
-when  it  involves  the  upper  end  of  the  lumbar  enlargement  the  reflex  of 
the  sole  is  exaggerated,  but  the  patellar  tendon-reaction  and  the  cremas- 
teric reflex  are  lost ;  and  when  the  lesion  is  situated  in  the  dorsal  region 
the  reflexes  of  the  sole,  of  the  cremaster,  and  of  the  patellar  tendon  are 
exaorserated. 

The  bladder,  rectum,  and  sexual  organs  are  generally  affected  in  acute 
myelitis.  At  first  there  may  be  spasmodic  closure  of  the  sphincter  of 
the  bladder,  so  that  a  catheter  has  to  be  used,  but  incontinence  of 
urine  soon  supervenes,  vesical  paralysis  being,  indeed,  sometimes  one 
of  the  earliest  symptoms  of  the  disease.  In  severe  cases  the  urine 
becomes  alkaline  and  sometimes  bloody  after  the  seventh  or  eighth  day  ; 
it  then  contains  numerous  crystals  of  the  triple  phosphates  and  putrefac- 
tion bacteria,  and  there  is  considerable  muco-purulent  deposit.  The 
bowels  are  obstinately  constipated,  and  the  abdomen  becomes  distended 
with  flatus,  while  soon  the  stools  are  passed  involuntarily.  Priapism  is 
not  an  uncommon  symptom  of  acute  myelitis,  the  erection  being  usually 
incomplete,  but  generally  persisting  for  days. 

The  vaso-vwtor  disturbances  are  variable.  The  paralyzed  limbs  are 
often  oedematous,  and  generally  cold,  although  occasionally  elevation  of 
temperature  has  been  observed  in  them.  The  perspiration  is  sometimes 
increased,  sometimes  diminished. 

The  trophic  disorders  consist  of  acute  bedsores,  which  may  make 
their  appearance  as  early  as  from  the  second  to  the  fifth  day  and  are 
situated  over  the  sacrum,  trochanters,  and  other  exposed  situations ; 
they  often  pursue  a  rapid  course  and  prove  fatal  by  pyaemia.  When  the 
disease  is  situated  in  the  lumbar  region  the  paralyzed  muscles  undergo 
a  diff"used  atrophy,  and  then  the  affected  nerves  and  muscles  manifest 
the  "  reaction  of  degeneration."  When  the  lesion  is  localized  in  the 
dorsal  region  the  muscles  retain  their  nutrition  and  the  electrical  reac- 
tions  are  normal. 

Psychical  symptoms  are  not  often  present  in  acute  myelitis,  although 
in  children  the  symptoms  may  be  ushered  in  by  headache,  delirium,  and 
general  convulsions ;  when  cerebral  symptoms  occur  in  the  adult  they 
are  probably  due  to  the  accompanying  fever. 

When  the  erector  muscles  of  the  spine  are  paralyzed  the  patient  is 
unable  to  sit  up  in  bed,  and  when  the  abdominal  muscles  are  paralyzed 
all  forcible  expiratory  acts  are  rendered  feeble,  and  consequently  the 
air-passages  cannot  be  cleared  of  mucus,  a  difficulty  which  is  still  further 
increased  when  the  intercostal  muscles  are  paralyzed.  When  the 
cervical  portion  is  implicated  some  or  all  of  the  muscles  of  the  upper 


550  MYELITIS. 

extremities  are  paralyzed  and  various  sensory  disorders  appear  in  them. 
In  addition  oculo-pupillary  symptoms  are  present,  and  double  optic- 
neuritis  lias  been  observed  on  rare  occasions  ;  while  the  pulse  may  either 
be  much  accelerated  or  retarded,  and  the  patient  suffers  from  palpitation, 
irregularity  of  the  heart's  action,  and  unpleasant  sensations  in  the  pre- 
cordial region. 

As  the  disease  ascends  the  movements  of  the  diaphragm  become 
feebler,  and  as  inspiration  is  now  carried  on  chiefly  by  means  of  the 
cervical  muscles  death  by  asphyxia  is  imminent;  when  the  medulla 
oblongata  becomes  involved  articulation  and  deglutition  are  interfered 
with,  and  the  patient  dies  from  respiratory  paralysis. 

In  acute  myelitis  the  early  stage  of  the  disease  is  accompanied  by 
fever,  and  the  temperature  may  remain  persistently  high  throughout  the 
whole  course  of  the  disease,  while  there  may  be  hyperpyrexia  at  death. 
In  other  cases  the  fever  is  slight  and  may  disappear  entirely  in  the 
course  of  the  disease,  but  in  the  tei'minal  stage  a  fever  of  remittent 
type  appears  which  is  caused  by  septic  infection  from  the  cystitis,  bed- 
sores, and  pyelo-nephritis. 

Acute  myelitis  is  always  rapidly  developed,  but  when  the  acute 
symptoms  have  subsided  the  disease  may  pass  into  a  chronic  myelitis, 
and  the  symptoms  may  then  remain  stationary  for  months  or  years. 
In  other  cases  acute  myelitis  pursues  an  ascending  course  and  becomes 
quickly  fatal.  When  the  lumbar  region  of  the  cord  is  the  chief  seat  of 
the  disease  it  proves  fatal  after  many  months  from  the  exhaustion  caused 
by  septic  fever.  In  some  cases  complete  recovery  may  take  place  and 
a  favorable  termination  may  occasionally  result  even  after  the  formation 
of  bedsores.  In  most  cases,  however,  recovery  is  only  partial,  and  one 
or  more  groups  of  muscles  remain  permanently  paralyzed  and  atrophied. 

Chronic  myelitis  is  sometimes  a  sequel  of  acute  myelitis,  but  in  most 
cases  the  disease  begins  slowly  and  is  gradually  developed.  The  symp- 
toms often  begin  by  parsesthesia  in  the  lower,  and  occasionally  in  the 
upper  extremities,  and  a  girdle  sensation,  and  at  the  same  time  the 
patient  complains  of  a  feeling  of  weakness  and  heaviness  of  the  limbs, 
and  probably  suffers  from  jerkings  of  the  legs  in  bed  at  night.  He 
also  complains  of  a  sensation  of  stiffness  of  the  legs,  which  is  worse  in 
the  morning  and  at  starting  to  walk  than  when  the  limbs  have  been 
moderately  exercised.  As  the  disease  advances  the  stiffness  and  weak- 
ness of  the  legs  become  worse,  and  after  a  time  the  paralysis  assumes 
the  typical  form  of  spastic  paraplegia,  or  occasionally  of  a  spinal  hemi- 
plegia, and  now  the  lower  half  of  the  body  is  also  more  or  less  anges- 
thetic.  The  course  of  chronic  myelitis  is  very  variable.  When  the 
disease  reaches  a  certain  degree  of  intensity  it  may  remain  stationary 


VARIETIES    OF    DIFFUSED    MYELITIS.  551 

for  mail}'  years,  or  periods  of  improvement  may  alternate  Avith  relapses 
and  exacerbations.  The  disease  may,  indeed,  last  a  lifetime  without 
producing  dangerous  symptoms.  Complete  recovery  is,  however,  rare 
and  the  majority  of  cases  terminate  fatally  either  from  bedsores,  cystitis 
and  pyiemia,  occasionally  from  bulbar  paralysis,  or  more  frequently 
from  pneumonia  or  other  intercurrent  disease. 


VARIETIES  OF  DIFFUSED  MYELITIS. 

The  following  varieties  of  diffused  myelitis  may  be  distinguished: 
1,  Central  myelitis;  2,  bulbar  myelitis;  3,  transverse  myelitis;  4, 
wounds  of  the  spinal  cord;  5,  compressive  myelitis;  6,  unilateral 
myelitis;  7,  meningo-myelitis;  8,  universal  progressive  myelitis;  and 
9,  disseminated  myelitis.  The  various  inflammations  of  the  spinal  cord 
may  be  subdivided  into  acute  and  chronic  myelitis. 


1.  Central  Myelitis. 

Symptoms. — This  affection  begins  suddenly  by  parsesthesise  and 
other  sensory  disturbances,  which  are  soon  followed  by  complete  anaes- 
thesia and  paralysis  with  flaccidity  of  the  lower  extremities,  and  by 
paralysis  of  the  bladder  and  rectum.  The  reflex  excitability  is  abol- 
ished, and  the  paralyzed  muscles  undergo  rapid  atrophy,  and  manifest 
the  "reaction  of  degeneration"  at  an  early  period.  The  further  prog- 
ress of  the  disease  is  marked  by  acute  bedsores,  cystitis  with  ammoni- 
acal  urine,  oedema  of  the  paralyzed  limbs,  arthropathies,  more  or  less 
intense  fever,  and  progressive  advance  of  the  paralysis  upwards,  so 
that  the  intercostal  muscles  and  those  of  the  upper  extremities  become 
successively  paralyzed,  and  ultimately  the  muscles  of  articulation  and 
deglutition  are  invaded,  and  the  patient  dies  from  respiratory  paralysis. 

The  course  of  acute  central  myelitis  is  very  similar  to  that  of  acute 
ascending  paralysis,  but  in  the  latter  the  bedsores  as  well  as  the  vesical 
and  rectal  disorders  of  the  former  disease  are  absent.  In  other  cases 
the  symptoms  become  more  or  less  chronic,  and  the  disease  may  then 
be  mistaken  for  chronic  atrophic  spinal  paralysis,  but  in  the  latter  dis- 
ease the  sensory  disorders  and  the  bedsores  of  the  former  affection  are 
wanting.  In  some  cases  the  symptoms  develop  with  almost  apoplecti- 
form rapidity,  the  lower  extremities  becoming  completely  paralyzed  in 
the  course  of  a  few  minutes,  or,  at  most,  in  the  course  of  an  hour  or 
two.     In  such  cases  the  gray  matter  of  the  cord  has  been  found  soft- 


552  MYELITIS. 

ened  and  mixed  with  red  blood-corpuscles,  and  the  disease  has  conse- 
quently been  named  hcematomyeUtis.  It  may  also  be  named  hypei-- 
acute  central  myelitis. 

2.  Bulbar  Myelitis. 

Symptoms. — Acute  bulbar  myelitis  begins  suddenly  with  violent 
headache,  giddiness,  vomiting,  distressing  hiccough,  various  pariTesthesijv?, 
and  difficulty  of  articulation  and  deglutition,  but,  contrary  to  what 
occurs  in  an  apoplectic  attack,  consciousness  is  retained.  After  a  short 
time  the  inferior  muscles  of  the  face,  the  muscles  of  tlie  tongue,  soft 
palate,  and  pharyngeal  muscles  become  paralyzed  in  various  degrees 
and  combinations,  and  in  some  cases  the  ocular  muscles,  especially  the 
external  recti,  may  be  implicated.  Disorders  of  respiration  appear  at 
an  early  period,  the  respirations  are  hurried  and  irregular,  and  there 
may  be  an  intense  feeling  of  oppression,  dyspnoea,  and  cyanosis. 
The  pulse  is  small,  quick,  and  irrc'gular  or  intermittent.  One,  two,  or 
all  the  extremities  may  be  paralyzed,  or  paralysis  of  the  limbs  may  be 
absent.  The  patient  may  complain  of  pain  and  formication  in  the 
limbs,  but  there  is  anesthesia.  The  bladder  and  rectum  may  become 
paralyzed  towards  the  terminal  period  of  the  disease.  Tlie  disturb- 
ances of  circulation  and  respiration  now  increase,  the  patient  becomes 
unconscious,  and  death  from  asphyxia  results. 

Chronic  projjressive  bulbar  paralysis  has  already  been  described. 
A  chronic  form  of  bulbar  paralysis  may  also  result  from  necrotic  pro- 
cesses, and  from  inflammation  set  up  by  tumors  and  other  morbid 
processes  in  the  neighborhood  of  the  meduHa,  but  this  form  of  bulbar 
myelitis  does  not  demand  separate  description. 

3.  Transverse  Myelitis, 

Symptoms. — Tlie  symptoms  of  transverse  myelitis  will  vary  accord- 
ing as  its  course  is  acute  or  chronic,  and  according  a.s  it  is  caused  by 
wounds  and  other  injuries  of  the  cord,  by  the  growth  of  tumors,  or  by 
the  extension  of  inflammation  from  other  tissues,  or  as  it  begins  as  an 
idiopathic  affection.  In  this  place,  however,  we  have  to  do  cliiefly  with 
the  localizing  symptoms,  and  for  the  purposes  of  description  the  affec- 
tion may  be  divided  into  a,  dorso-lumbar ;  6,  dorsal;  and  c,  cervical 
transverse  myelitis. 

a.  Dorso-lumbar  transverse  myelitis  may  begin  more  or  less  sud- 
denly by  fever,  par?esthesia  of  the  lower  extremities,  retention  of  urine, 


VARIETIES    OF    DIFFUSED    MYELITIS.  553 

and  startings  of  the  lower  extremities,  but  tliese  symptoms  soon  give 
place  to  sensory  and  motor  paralysis  of  the  limbs  and  paralysis  of  the 
sphincters  of  the  bladder  and  rectum.  The  lower  extremities  become 
(edematous,  and  their  muscles  may  undergo  a  diffused  atrophy,  and 
may  manifest  the  reaction  of  degeneration.  The  patellar  tendon-reac- 
tions, which  were  possibly  at  first  exaggerated,  now  become  lost,  and 
the  cremasteric  reflex  is  also  lost,  but  the  reflex  of  the  sole  is  often 
exaggerated.  The  neck  of  the  femur  is  occasionally  the  subject  of 
spontaneous  fracture,  and  arthropathies  of  other  joints  may  appear. 
In  acute  cases  of  this  kind  the  patient  generally  dies  at  an  early  period 
of  the  disease  from  the  usual  cystitis,  bedsores,  and  septic  fever. 

The  ehronif  form  of  the  disease  begins  gradually  by  girdle  pains  in 
the  region  of  distribution  of  the  ilio-hypogastric  and  ilio-inguinal  nerves, 
while  the  patient  complains  of  shooting  pains,  and  various  par^esthesise 
in  the  lower  extremities.  The  patient  suffers  from  cramps  in  the  calves 
of  the  legs,  and  is  soon  fatigued,  while  the  movements  are  stiff"  and 
constrained.  After  a  time  the  lower  extremities  become  rigid  by  con- 
tractures, the  cutaneous  reflexes  and  tendon-reactions  are  exaircrerated 
in  them,  and  the  gait  is  of  the  spastic  variety.  As  the  disease  advances 
the  sensory  disorders  become  more  profound,  and  anaesthesia  of  the 
lower  extremities  becomes  established,  while  the  patient  becomes  com- 
pletely paraplegic.  The  lesion  now  usually  invades  the  lumbar  enlarge- 
ment, and  when  it  creeps  down  to  the  level  of  the  second  or  third 
lumbar  nerves  the  cremasteric  reflex  is  lost,  the  extensor  muscles  of 
the  knee  undergo  atrophy,  the  patellar  tendon-reaction  is  abolished, 
and  the  sphincters  are  soon  afterwards  paralyzed.  AVith  a  still  further 
downward  extension  of  the  lesion  all  the  muscles  of  the  lower  extremi- 
ties undergo  a  diffused  wasting  and  lose  their  tension  :  the  limbs  become 
oedematous,  the  reflex  of  the  sole  may,  after  a  time,  be  lost ;  bedsores, 
which  have,  indeed,  already  appeared  over  the  sacrum,  now  form  over 
the  trochanter  and  other  points  subjected  to  pressure;  the  urine  is 
alkaline  and  contains  pus ;  and  the  patient  dies  from  pyaemia. 

b.  Dorsal  Transverse  3Iyelitis. — In  this  form  of  myelitis  both  the 
sensory  and  motor  paralysis  extend  higher  than  in  the  dorso-lumbar 
variety,  but  the  condition  of  the  lower  extremities,  with  regard  to  paral- 
ysis, contractures,  spastic  gait,  exaggerated  reflexes,  and  tendon-reac- 
tions, is  the  same  as  in  the  early  stage  of  that  disease.  When  the 
lesion  is  situated  in  the  upper  part  of  the  dorsal  region  the  muscles  of 
the  back  and  abdomen  are  liable  to  be  paralyzed,  and  paralysis  of  the 
abdominal  muscles  renders  urination,  defecation,  and  forcible  expiratory 
acts  difficult,  and  consequently  the  patient  is  troubled  with  constipation, 
and  being;  unable  to  clear  the  bronchial  tubes  thorougldv  from  mucus 


554  MYELITIS, 

he  is  liable  to  succumb  to  a  slight  bronchial  catarrh.  Double  optic 
neuritis  has  occasional^  been  observed.  The  level  at  which  the  cord 
is  diseased  may  be  determined  by  the  level  of  the  girdle  pains  and 
anaesthesia,  and  by  an  examination  of  the  cremasteric,  gluteal,  abdomi- 
nal, epigastric,  dorsal,  and  scapular  reflexes. 

c.  Cervical  Transverse  Myelitis. — This  form  of  myelitis  generally 
begins  with  pain  in  the  back  of  the  neck,  and  the  muscles  of  the  neck 
become  rigid,  while  owing  to  the  predominant  action  of  those  of  the 
back,  often  of  one  side,  the  head  is  generally  rotated  and  retracted. 
The  upper  extremities  now  become  subject  to  shooting  pains  and  muscular 
startings,  provided  the  lesion  involves  the  origin  of  the  brachial  plexus, 
but  these  symptoms  of  irritation  soon  give  place  to  sensory  and  motor 
paralysis.  The  paralysis  of  the  upper  extremities  is  of  the  atrophic 
variety,  and  its  distribution,  with  the  consequent  deformities,  will  de- 
pend upon  the  level  of  the  lesion,  while  it  may  be  accompanied  by 
oedema  and  arthropathies.  The  lower  extremities  become  affected  with 
a  spasmodic  paralysis  with  exaggerated  reflexes  and  tendon-reaction. 
There  may  also  be  complete  or  incomplete  anaesthesia  of  the  body  and 
lower  extremities  below  the  level  of  the  lesion,  and  of  the  upper  ex- 
tremities on  a  level  with  the  lesion,  the  distribution  of  the  last  depend- 
ing upon  the  posterior  roots  which  are  implicated.  The  pupils  arc,  in 
some  cases,  dilated,  in  others  contracted,  or  often  first  dilated  and  then 
contracted;  the  size  of  the  palpebral  fissure  may  be  increased  or  dimin- 
ished; and  the  face  may  be  unusually  pale  or  flushed,  and  it  is  often 
covered  by  perspiration.  In  some  cases  oculo-pupillary  symptoms  are 
absent.  The  establishment  of  paralysis  may  be  preceded  by  anoma- 
lous symptoms  like  cough,  dyspnoea,  sweats,  wasting  of  the  muscles  of 
the  arm  and  neck,  pains  between  the  shoulders  or  at  the  back  of  the 
neck,  severe  attacks  of  vomiting,  hiccough,  difficulty  of  deglutition,  and 
great  slowness  of  the  pulse.  The  inflammatory  process  is  liable  to 
ascend  to  the  medulla  oblongata,  and  death  results  from  respiratory 
paralysis. 

4.  Wounds  of  the  Spinal  Cord. 

Symptoms. — The  symptoms  caused  by  wounds  and  injuries  of  the 
cord  may  be  divided  into  (a)  those  caused  by  comparatively  slight 
nijuries  of  the  cord,  such  as  simple  incised  and  punctured  wounds, 
and  {h)  those  caused  by  the  more  serious  lesions,  such  as  sudden  com- 
pression and  tearing  of  the  cord. 

a.  The  symptoms  which  indicate  that  an  injury  by  cutting  or  stal)- 
bing  in  the  neighborhood  of  the  spine  has  penetrated  the  cord  will 
at  first  be  those  caused  by  loss  of  conduction  to  and  from  the  brain 


VARIETIES    OF    DIFFUSED    MYELITIS.  555 

in  the  portions  situated  below  the  seat  of  the  injury.  At  the  moment 
the  injury  is  received  paraplegia,  hemiparaplegia,  or  general  paralysis 
is  suddenly  developed.  If  the  cord  is  completely  divided,  there  is  com- 
plete anaesthesia  of  the  paralyzed  parts ;  but  if  only  one-half  of  the 
cord  is  divided  the  anaesthesia  is  situated  on  the  side  opposite  to  the 
lesion,  Avhile  girdle  pains  may  be  present  on  a  level  with  the  lesion. 
If  the  injury  be  of  considerable  extent  paralysis  of  the  bladder  and 
rectum  occurs,  and  there  is  also  vaso-motor  paralysis  with  increased 
temperature  and  redness  of  the  region  affected  by  the  motor  paralvsis. 
The  reflex  actions  are  usually  abolished  at  first,  owing  to  the  shock,  but 
if  the  lesioii  is  situated  in  the  dorsal  or  cervical  region,  they  may, 
subsequently  be  exaggerated.  After  a  time  the  symptoms  of  secondary 
traumatic  myelitis  complicate  those  caused  by  the  primary  lesion,  and 
then  the  symptoms  will  be  more  or  less  like  those  caused  by  acute 
idiopathic  transverse  myelitis. 

h.  The  symptoms  which  indicate  that  the  cord  is  crushed  or  torn  in 
severe  injuries  of  the  spine  are,  in  addition  to  the  evidences  of  local 
injury  of  the  spine,  complete  paralysis  and  anaesthesia  of  the  portion  of 
the  body  which  lies  below  the  seat  of  the  injury.  The  other  symptoms 
are  abolition  of  the  reflex  actions,  retention  of  urine  and  constipation, 
with  meteorism  or  involuntary  evacuations  of  urine  and  feces,  priapism, 
in  which  the  organ  is  turgid  but  still  flexible,  and  elevation  or  some- 
times depression  of  the  temperature  of  the  body. 

When  the  cervical  region  is  injured  the  temperature  of  the  body  is 
generally  much  increased,  and  often  rises  still  further  for  some  hours 
after  death.  In  a  case  of  fracture  of  the  fifth  and  sixth  cervical  ver- 
tebr;:©,  reported  by  Quincke,  the  temperature  at  death  was  42.3°  C, 
and  eight  hours  after  death  it  was  43,2°  C,  and  in  a  case  of  compres- 
sion of  the  cervical  region  he  found  the  temperature  42,7°  C,  at  death, 
and  43.6°  C,  eight  hours  afterwards,  A  case  of  fracture  of  the  spine 
on  a  level  with  the  body  of  the  fifth  cervical  vertebra  is  recorded  by 
Mr,  Jonathan  Hutchinson,  in  which  the  temperature,  which  was  99,3°  F. 
in  the  urethra  twent^^-four  hours  after  the  injury,  rose  to  106.3°  F.  at 
death,  thirty-eight  hours  after  the  injury,  and  Mr.  F.  Churchill  has 
recorded  a  case  of  fracture  of  the  same  vertebra  in  which  the  tempera- 
ture in  the  axilla  was  110°  soon  after  death.  In  some  cases  the  tem- 
perature undergoes  great  variations,  being  in  one  case  as  low,  at  one 
time,  as  94.2°  F.,  and  soon  afterwards  as  high  as  106.4°  F.,  these  varia- 
tions being  apparently  independent  of  bedsores  and  septic  fever.  In 
some  cases  of  fracture  of  the  cervical  spine  the  temperature  of  the 
body  falls  after  the  injury,  and  remains  low  till  death. 

Another  symptom  of  injury  of  the  cervical  region  is  afforded  by  a 


556  MYELITIS. 

very  feeble,  slow,  and  infrequent  pulse,  which  beats  in  some  cases  only 
forty- eight  times  in  the  minute,  and  it  is  in  these  cases,  according  to  Mr. 
Jonathan  Hutchinson,  that  the  temperature  flills  and  the  surface  is  cold 
to  the  touch.  When  the  injury  is  situated  in  the  dorsal  or  lumbar 
region  the  pulse  is  not  affected  except  by  the  shock,  just  as  occurs 
after  other  severe  accidents.  The  severer  forms  of  injury  to  the  cervi- 
cal spine  are  rapidly  fatal  by  paralysis  of  respiration,  but  when  the 
patient  survives  for  a  few  days  the  symptoms  of  acute  transverse  mye- 
litis are  superadded  to  those  caused  by  the  injury. 

5.  Compression  Myelitis,  Tumors  in  the  Vertebral  Canal. 

Symptoms. — The  symptoms  of  compression  myelitis  nuiy  be  divided 
into  a,  extrinsic,  and  h,  intrinsic  sym])toms. 

a.  The  extrinsic  or  prodromal  symptoms  consist  of  severe  girdle 
pains,  hypersesthesia  of  the  skin  corresponding  to  the  distribution  of 
the  pain,  eccentric  neuralgiform  pains  generally  fixed  to  one  spot,  severe 
pain  in  the  back,  local  stifiness,  and  tenderness  of  the  spinous  processes. 
The  neuralgic  pains  are  sometimes  accompanied  by  herpetic  or  bullous 
eruptions  of  the  skin.  Phenomena  of  motor  irritation  are  superadded 
to  the  sensory  disturbances  in  the  distribution  of  the  nerves  whose  roots 
were  first  implicated.  These  consist  of  twitchings,  spasms,  and  con- 
traction of  the  muscles  supplied  by  the  affected  nerves.  The  irritative 
motor  symptoms  are  soon  followed  by  weakness  and  paralysis  of  single 
muscles  or  groups  of  muscles,  the  affected  muscles  undergo  a  diffused 
atrnpliy,  the  cutaneous  reflex  actions  and  the  tendon  reactions  are  lost 
in  them,  and  they  may  manifest  the  partial  "  reaction  of  degeneration," 
but  not  often  the  severest  form  of  that  reaction.  As  the  second  stage 
of  the  disease  approaches  the  patient  complains  of  pan\?sthesia3  in  the 
lower  half  of  the  body,  consisting  of  tingling,  numbness,  and  sensations 
of  heat  or  of  cold,  and  after  a  time  more  or  less  ansesthesia  is  established, 
but  complete  anesthesia  is  rare  in  vertebral  caries.  The  motor  symp- 
toms consist  at  this  stage  of  startings  of  the  lower  extremities,  especially 
at  night,  and  a  sense  of  weariness  and  heaviness  of  the  limbs,  while  the 
patellar  tendon-reactions  will  often  be  found  exaggerated,  unless  the 
lesion  is  situated  in  the  lower  dorsal  and  lumbar  regions,  when  they  may 
be  lost. 

When  cancer  of  the  vertebral  column  makes  its  way  into  the  spinal 
canal  it  gives  rise  to  the  most  agonizing  pains.  These  consist  of  severe 
girdle  pains,  and  of  pains  which  radiate  along  the  distribution  of 
certain  nerves,  such  as  the  crural  and  sciatic  nerves,  when  the  lumbar 
vertebrae  are  affected.     The  skin  to  Avhich  the  affected  nerves  are  dis- 


VARIETIES    OF    DIFFUSED    MYELITIS.  557 

tributed  is  intensely  hyperresthetic,  so  that  the  slightest  touch  is  painful. 
The  pains  never  intermit,  but  they  are  liable  to  paroxysmal  exacerba- 
tions of  great  severity,  which  are  difficult  to  allay  even  by  laro-e  doses 
of  narcotics.  Patches  of  angesthesia  may  be  observed  in  the  skin  to 
-which  the  affected  nerves  are  distributed,  but  the  pain  still  continues 
unabated,  this  condition  being  named  ancesthesia  dolorosa,  and  when 
the  symptoms  of  transverse  myelitis  are  after  a  time  superadded  to  these 
sensory  disorders,  the  condition  is  called  paraplegic  dolorosa. 

In  all  cases  in  which  the  premonitory  symptoms  of  compression  or 
transverse  myelitis  are  present  a  careful  examination  must  be  made  to 
determine  the  level  of  the  girdle  sensations,  or  the  upper  limit  of  the 
pan^sthesia  or  anaesthesia  if  any  be  present,  and  when  once  this  point 
has  been  ascertained  the  vertebral  column  on  a  level  with  the  upper 
limit  of  the  sensory  disorders  must  be  subjected  to  careful  examination. 
In  cases  of  angular  curvature,  and  in  those  cases  in  which  an  external 
tumor  has  made  its  way  into  the  vertebral  canal,  decided  evidence  of  the 
nature  of  the  disease  may  be  at  once  obtained.  And  even  in  those  cases 
in  which  there  are  no  enlargements  or  other  deformities  it  may  be  found 
that  one  or  two  of  the  spinous  processes  are  tender  to  pressure  or  percus- 
sion, or  sensitive  to  a  hot  sponge  drawn  along  the  vertebral  column,  or 
to  the  cathode  of  the  galvanic  current. 

b.  The  intrinsic  syinptonis  are  generally  the  same  as  those  of  trans- 
verse myelitfs,  and  are  ushered  in  by  paralysis  of  the  lower  extremities, 
Avhich  may  begin  at  first  as  a  hemiparaplegia,  and  afterwards  develop 
into  complete  paraplegia.  The  symptoms  of  acute  and  chronic  trans- 
verse myelitis  need  not  be  described  a  second  time.  In  intramedullary 
tumors  the  phenomena  of  atrophic  paralysis  may  predominate,  but  they 
are  often  associated  with  a  spasmodic  paralysis  with  exaggerated  reflexes 
in  one  of  the  limbs  or  in  one  or  more  groups  of  muscles.  Multiple 
tumors  are  sometimes  found  in  the  cord,  consisting  of  sarcoma,  tubercle, 
or  syphilis,  and  the  symptoms  may  then  manifest  themselves  at  dif- 
ferent elevations,  as  in  acute  and  chi'onic  disseminated  myelitis.  In 
addition  to  the  variable  character  of  the  purely  spinal  symptoms,  one 
or  more  of  the  tumors  may  appear  in  the  medulla  oblongata  and 
pons,  and  the  symptoms  caused  by  these  tumors  may  help  to  clear  the 
diagnosis. 

6.  Spinal  Hemiplegia  and  Hemiparaple(!Ia  (Unilateral  Lesion 
OF  THE  Spinal  Cord). 

Symptoms. — The  symptoms  of  unilateral  spinal  paralysis  may  be 
developed   insidiously  and  gradually,  or  (juite  suddenly,  the  mode  of 


558  MYELITIS. 

invasion  depending  upon  whether  the  lesion  consists  of  a  slowly  invad- 
ing disease  like  the  growth  of  a  tumor,  or  upon  a  sudden  injury  like 
a  stab  from  a  sharp-pointed  instrument.  The  most  prominent  symptoms 
are  a  motor  paralysis  on  the  side  of  the  lesion  which  may  involve  only 
one  leg  (hemiparaplegia),  or  the  leg  and  the  arm  of  the  same  side  (spinal 
hemiplegia),  and  a  sensory  paralysis  on  the  opposite  side  of  the  body. 

The  paralyzed  muscles  undergo  early  and  rapid  atrophy  when  the 
lesion  is  situated  in  the  lumbar  enlargement,  but  when  it  is  situated  at 
a  higher  level  the  lower  extremity  on  the  side  of  the  lesion  undergoes 
spasmodic  paralysis,  provided  the  patient  survive  sufficiently  long  for 
secondary  degenerations  to  occur  in  the  cord,  while  groups  of  the  muscles 
of  the  upper  extremity  are  the  subjects  of  atrophic  paralysis  if  the 
lesion  is  on  a  level  with  the  roots  of  origin  of  the  In-achial  plexus.  In 
some  cases  well-marked  ataxia  has  been  observed  in  the  paralyzed  leg 
after  return  of  motor  power, 

Vaso-motor  paralysis  is  declared,  on  the  side  of  the  lesion,  by  an 
elevation  of  the  temperature  of  the  paralyzed  limb  to  the  extent  of 
from  1°  F.  to  3.6°  F.,  but  the  temperature  may  be  lower  than  normal 
when  the  disease  has  existed  for  some  time. 

Muscular  sense  and  muscular  sensibility  are  also  usually  diminished 
on  the  side  of  the  lesion,  but  all  forms  of  cutaneous  sensibility  are 
increased.  Impressions  of  touch,  temperature,  and  pain  are  felt  with 
unusual  acuteness,  and  there  is  an  increased  power  of  localizing  tactile 
sensations.  At  times,  however,  the  hypersesthesia  is  limited  to  a  few 
forms  only  of  cutaneous  sensibility.  The  hyperjesthetic  area  of  the 
skin  is  usually  bounded  by  an  anesthetic  zone  which  corresponds  with 
the  level  and  longitudinal  extent  of  the  lesion  of  the  spinal  cord,  and  a 
narrow  hypertesthetic  belt  which  extends  to  the  opposite  side  may  some- 
times be  detected  above  the  anaesthetic  zone  (Fig.  171).  The  reflex 
actions  on  the  side  of  the  motor  paralysis  vary,  but  they  are  generally 
increased  below  the  seat  of  the  lesion. 

On  the  side  opposite  the  lesion  there  are  no  motor  disorders  or  they 
are  only  slight  in  degree,  and  both  the  muscular  sense  and  the  electro- 
muscular  sensibility  are  retained  on  that  side ;  however,  there  is  more 
or  less  complete  anesthesia  of  the  skin,  although  some  forms  of  sensi- 
bility may  be  involved  to  a  greater  extent  than  others.  The  anesthesia 
extends  nearly  to  the  median  line  of  the  body  and  it  is  often  bounded 
above  by  a  slightly  hyperesthetic  region,  corresponding  to  a  similar 
zone  on  the  opposite  side.  Near  the  median  line  anteriorly  and  pos- 
teriorly there  is  a  vertical  space  of  about  one  inch  in  breadth  in  which 
hyperesthesia  is  absent  on  the  side  of  the  lesion,  and  a  similar  space 
on  the  front  and  back  in  wdiich  there  is  an  absence  of  any  great  degree 


VARIETIES    OF    DIFFUSED    MYELITIS, 


559 


of  anaesthesia,  these  phenomena  finding  a  sufficient  explanation  in  the 
well-known  anatomical  fact  that  the  sensory  nerves  of  the  two  sides 
overlap.  There  are  no  vaso-motor  disturbances  on  the  anaesthetic  side, 
and  reflex  action  is  usually  normal,  but  has  occasionally  been  found 
increased.  The  patient  sometimes  complains  of  a  feeling  of  constriction 
and  neuralgiform  pains  on  a  level  with  the  lesion,  and  these  may  at 
times  be  more  prominent  on  the  anaesthetic  and  at  other  times  on  the 
hyperaesthetic  side.     In  acute  traumatic  cases  retention  or  incontinence 


Diagram  of  the  Cutaneous  Symptoms  in  Unilateral  Lesion  of  the  Dorsal  Portion  of  the 
Spinal  Coed  on  the  Left  Side.     (After  Erb.) 
The  diagonal  shading  (a)  signifies  motor  and  vaso-motor  paralysis;  the  vertical  shading  (6,  d)  signifies 
cutaneous  antesthesia;  the  dotted  shading  (a,  c)  indicates  hyperesthesia  of  the  skin. 

is  always  present  at  first,  but  after  a  time  recovery  takes  place,  so  that 
at  most  only  a  certain  degree  of  weakness  of  the  sphincters  remains. 
The  sexual  functions  are  at  times  unaffected  and  at  other  times  more  or 
less  weakened. 

The  trophic  disorders  consist  of  acute  bedsores  which  appear  on  the 
anaesthetic  side,  and  inflammation  of  the  knee-joint,  which  appears  on 
the  paralyzed  side. 


560  '         MYELITIS. 

Varieties. — The  symptoms  differ  according  to  the  level  at  Avhich  the 
lesion  is  situated  in  the  cord. 

(1)  Unilateral  lesion  of  the  lumbar  eiilargement  causes  an  anaes- 
thetic zone,  on  the  paralyzed  side,  in  the  area  of  distribution  of  one  or 
more  of  the  sensory  branches  of  the  sacral  or  lumbar  plexuses,  in  addi- 
tion to  the  other  characteristic  unilateral  symptoms,  but  there  is  no 
belt  round  the  body.  The  muscles  of  the  paralyzed  limb  undergo 
atrophv  when  the  lesion  occupies  a  considerable  portion  of  the  lumbar 
enlargement  in  A'ertical  extent. 

(2)  Unilateral  lesions  of  the  dorsal  re<jion  of  the  cord  give  rise  to 
the  most  characteristic  symptoms  of  the  disease,  as  already  described. 

(3)  Unilateral  lesions  of  the  cervical  2>ortion  give  rise  to  different 
symptoms  according  to  the  level  at  which  the  lesion  is  situated.  The 
motor  and  sensory  disorders  are  the  same  in  the  trunk  and  lower  ex- 
tremities as  when  the  dorsal  region  is  affected,  but  when  the  lesion  is 
situated  on  a  level  with  the  brachial  plexus  the  muscles  of  the  upper 
extremity  undergo  atr()i)hic  jiaralysis,  while  hyperaesthesia  of  certain 
parts  of  the  skin  is  mingled  with  anaesthesia  of  other  regions,  or  for 
certain  varieties  of  sensation.  On  the  side  opposite  the  lesion  there  is  no 
paralysis,  but  there  is  complete  anaesthesia  of  the  parts  below  the  level 
of  the  lesion.  In  addition  to  these  symptoms  oculo-pupillary  phenomena 
and  vaso-motor  paralysis  of  the  side  of  the  face  are  present  on  the 
side  of  the  lesion.  If  the  lesion  is  situated  in  the  upper  part  of  the 
cervical  region,  the  neck  and  head  on  the  side  of  the  lesion  manifest 
annesthesia  and  hypenvstliesia  of  certain  areas  of  the  skin,  and  paral- 
ysis of  the  vaso-motor  and  oculo-pupillary  fibres,  while  on  the  opposite 
side  there  are  usually  an«sthesia  of  the  neck  and  a  narrow  zone  of 
hyperiTSSthesia,  with  a  normal  condition  of  the  face  and  eye. 

7.  Meninoo-myelitis. 

Myelitis  is  sometimes  complicated  by  the  symptoms  of  meningitis. 
The  symptoms  Avhich  indicate  meningitis  are  pain  and  stiffness  in  the 
back  of  the  neck,  pronounced  hyperesthesia,  diffused  pains  in  the  back 
and  lower  extremities,  pain  along  the  vertebral  column,  and  tenderness 
on  pressure  of  some  of  the  spinous  processes  of  the  vertebrae.  In  some 
chronic  cases  the  posterior  are  more  involved  than  the  lateral  columns, 
and  then  ataxic  symptoms  predominate  over  those  of  paralysis. 

8.  Universal  Progressive  Myelitis. 

This  form  of  myelitis  embraces  the  whole  transverse  area  of  the  cord, 
and  is  characterized  by  a  progressive  weakness  of  the  lower  extremities 


VARIETIES    OF    DIFFUSED    MYELITIS.  561 

-which  develops  into  complete  paralysis.  The  disease  usually  begins  in 
the  lower  extremities  and  pursues  an  ascending  course,  but  occasionally 
it  begins  in  the  upper  extremities  and  pursues  a  descending  course. 
The  muscles  may  be  in  a  state  of  contracture  at  first  but  as  the  gray 
matter  becomes  involved  they  undergo  gradual  atrophy.  The  cuta- 
neous reflexes,  tendon-reactions,  and  faradic  contractility  also  gradualh^ 
diminish  and  gradually  disappear.  There  may  be  more  or  less  violent 
pains  in  the  back,  trunk,  and  extremities,  the  patient  complains  of 
paraesthesiae  and  dysaesthesiee,  and  after  a  time  there  is  complete  anaes- 
thesia, paraplegia,  paralysis  of  the  sphincters,  and  bedsores. 

9.  Disseminated  Myelitis. 

Symptoms. — There  are  two  forms  of  disseminated  myelitis,  a,  the 
acute;  h,  the  chronic. 

The  symptoms  of  the  acute  form  are  very  variable,  but  sensibility  is 
usually  more  or  less  impaired,  and  there  is  a  spasmodic  paralysis  of  the 
lower  extremities  with  its  attendant  phenomena,  although  in  some  cases 
one  or  more  groups  of  muscles  may  suffer  from  an  atrophic  paralysis. 
The  state  of  the  electrical  sensibility  and  of  the  cutaneous  reflexes  is 
variable,  but  they  are  generally  diminished.  The  grouping  of  the 
symptoms  may  show  that  several  centres  of  disease  exist,  and  the  diag- 
nosis is  rendered  more  probable  if  the  symptoms  of  acute  myelitis 
supervene  during  an  attack  of  variola,  or  if  they  develop  suddenly  in 
phthisical  patients. 

Chronic  disseminated  myelitis  is  a  part  of  a  disease  which  is  widely 
distributed  in  the  spinal  cord  and  brain,  and  will  be  subsequently  de- 
scribed under  the  name  of  multiple  sclerosis. 

Morbid  Anatomy  and  Physiology. — The  morbid  anatomy  of  the 
various  forms  of  myelitis  has  already  been  sufficiently  considered,  and 
we  shall  now  make  a  few  remarks  to  connect  the  morbid  changes  with 
the  principal  alterations  of  function  observed  in  this  disease. 

Acute  myelitis  gives  rise  to  the  various  forms  of  softening  of  the 
spinal  cord  which  have  already  been  described.  The  initial  symptoms 
of  irritation,  which  are  present  in  the  early  stages  of  acute  myelitis,  must 
be  ascribed  to  the  increased  irritability  of  the  nerve  cells  and  fibres, 
occasioned  by  increased  nutritive  activity  during  the  early  stages  of  the 
inflammatory  process,  while  the  later  symptoms  of  paralysis  ai-e  caused 
by  the  destruction  of  these  elements  and  their  compression  by  inflam- 
matory exudation.  The  girdle  pains  are  caused  by  implication  of  the 
posterior  roots  of  the  dorsal  region  in  the  inflammatory  process,  while 
the  partesthesiae  and  neuralgic  pains  of  the  inferior  half  of  the  body 

36 


562  MYELITIS. 

result  from  irritation  of  the  sensory  conducting  paths  situated  in  the 
gray  matter  and  posterior  cokimns  of  the  cord.  The  motor  symptoms 
are  caused  first  by  irritation  and  subse(][uently  by  loss  of  the  function  of 
the  motor  centres  and  conducting  fibres  in  the  cord.  When  the  anterior 
gray  horns  are  diseased  the  resulting  paralysis  is  of  the  atrophic  and 
when  the  pyramidal  tracts  are  affected  the  paralysis  is  of  the  spasmodic 

variety. 

When  the  myelitis  affects  the  lumbar  region  the  bladder  and  rectum 
are  involved,  the  sphincters  being  first  closed  by  spasm,  and  subsequently 
incompetent  from  paralysis.  Priapism  must  be  regarded  as  a  sign  of 
irritation  produced  either  by  interference  with  the  conducting  paths 
passing  from  the  brain  to  the  lumbar  portion  of  the  cord,  or  by  reflex 
irritation  proceeding  from  the  bladder  or  skin.  The  trophic  affections 
of  the  muscles  and  bones  are  caused  by  lesion  of  the  ganglion  cells  of 
the  anterior  horns,  while  the  cutaneous  trophic  affections  and  bedsores 
appear  to  be  caused  by  disease  of  the  posterior  horns.  The  vaso-motor 
disturbances  are  caused  by  interference  with  the  centres  in  the  cord, 
but  the  spinal  mechanisms  which  preside  over  these  functions  are  not 
yet  clearly  ascertained. 

In  acute  central  myelitis  the  softening  affects  principally  the  gray 
substance,  which  often  flows  out  or  becomes  depressed  under  the  surface 
of  section  Avhen  the  cord  is  divided  transversely.  On  microscopic  ex- 
amination the  disease  is  seen  to  extend  in  the  lumbar  region  forwards 
from  the  central  column  into  the  anterior  gray  horns,  the  ganglion  cells 
of  which  may  be  entirely  destroyed  and  also  backwards  into  tlie  posterior 
gray  horns,  while  in  some  cases  the  white  substance,  especially  the 
pyramidal  tracts,  may  be  implicated  in  the  disea.se.  In  the  cervical  and 
upper  dorsal  regions  of  the  cord  and  in  the  medulla  oldongata  the  disease 
is  restricted  to  the  central  gray  column  and  the  accessory  cells  of  the 
anterior  gray  horns  and  their  continuations  through  the  medulla,  while 
the  fundamental  cells  in  these  regions  may  be  entirely  unaffected. 
Hcemato myelitis  is  like  acute  central  myelitis  in  every  respect  except 
that  in  the  former  of  the  two  the  central  softened  mass  assumes  a 
hemorrhagic  character.  In  the  cases  of  acute  bulbar  myelitis  observed 
by  Leyden,  small  indefinite  centres  of  softening  were  found  in  the 
medulla  oblongata. 

In  acute  transverse  myelitis  the  part  of  the  cord  in  which  the  chief 
lesion  is  localized  is  found  in  various  stages  of  softening,  and  if  the 
case  has  assumed  a  more  or  less  chronic  form  the  usual  ascending  and 
descending  degenerations  are  observed  above  and  below  the  primary 
seat  of  the  disease.  In  rapidly  fatal  cases  evidences  of  inflammation 
are  discovered  in  the  gray  matter  above  and  below  the  seat  of  the  chief 


VARIETIES    OF    DIFFUSED    MYELITIS. 


563 


lesion.  In  the  neighborhood  of  the  primary  lesion  all  the  ganglion  cells 
of  the  anterior  horns  may  be  destroyed,  but  in  the  remote  portions  of 
the  cord  the  disease  becomes  more  and  more  limited  to  the  central  o-ray 
columns  and  to  the  margins  of  the  groups  of  ganglion  cells  in  the 
anterior  horns.  The  annexed  diagram  (Fig.  172)  illustrates  this  condi- 
tion, and  although  it  was  taken  from  a  somewhat  protracted  case  of 
myelitis,  I  have  observed  similar  appearances  in  the  cervical  region  from 
a  case  of  fracture  of  the  vertebral  column  in   the  dorsal  region  which 

Fig.  172. 


Section  of  the  Middle  or  the  Cervical  Enlargement  of  the  Spinal  Cord  from  a  Case  of 
Central  Myelitis.    (After  Young  ) 

i,  The  internal  ;  a,  the  anterior;  al,  the  antero-lateral  ;  &nd pi,  the  pustero-lateral  group.  The  median 
area  was  completely  destitute  of  cells,  and  a  large  number  of  the  marginal  cells  of  the  different  groups  of 
the  anterior  horn  were  destroyed  or  diseased. 


proved  fatal  in  five  days.  The  continuation  of  the  central  column  into 
the  medulla  olilongata  and  its  accessory  nuclei  are  generally  implicated. 
In  simple  incised  or  punctured  wounds  of  the  spinal  cord  the  cut  edges 
project  at  first  beyond  the  pia  and  the  wound  is  closed.  In  a  few  days 
the  membranes  are  reddened  and  covered  with  fibro-purulent  matter, 
while  the  neighboring  parts  of  the  cord  are  more  or  less  softened.  Crush- 
ing of  the  cord  causes  softening  and  disintegration  of  the  cord  itself,  and 
congestion  and  hemorrhage  into  the  membranes.  If  the  patient  survive 
a  kind  of  cicatrix  is  formed  which  may  enclose  cystic  cavities  containing 


564  MYELITIS. 

clear  fluid.  In  acute  myelo-meningitis  the  usual  signs  of  meningitis 
will  be  found  along  with  those  of  myelitis,  and  in  sections  of  the  cord 
tinted  with  carmine  a  highly  stained  border  is  observed  which  extends 
more  or  less  deeply  into  the  substance  of  the  cord  and  consequently  this 
form  of  disease  has  been  called  peripheric  or  cortical  myelitis.  Acute 
disseminated  myelitis  occurs  in  small  spots  scattered  through  the  sub- 
stance of  the  cord.  The  morbid  change  appears  to  consist  chiefly  of 
an  increase  of  the  interstitial  tissue,  which  becomes  unusually  dense  and 
rich  in  nuclei. 

.  Chronic  myelitis  gives  rise  to  gray  degeneration  or  sclerosis  of  the 
aff"ected  parts,  although  the  cord  is  sometimes  found  softened  in  the 
main  focus  of  disease.  The  connection  between  the  morbid  changes 
and  the  symptoms  is  the  same  as  in  acute  myelitis.  In  chronic  cen- 
tral myelitis  the  disease  appears  apparently  as  an  acute  central  myelitis, 
and  then  assumes  the  chronic  form.  It  may  pursue  an  ascending 
course,  but  it  is  not  so  surely  invading  as  Landry's  paralysis.  The 
morbid  appearances  are  the  same  as  those  found  in  other  forms  of  cen- 
tral myelitis,  but  in  addition  the  white  substance  is  invaded  in  the 
lumbar  region,  the  columns  of  Goll  and  the  direct  cerebellar  tracts 
undergo  an  ascending  sclerosis,  and  the  lateral  columns  in  the  lumbar 
region  a  descending  sclerosis.  This  disease  may  be  set  up  by  an  injury 
of  the  sciatic  nerve  or  by  the  pressure  of  a  tumor  on  the  cauda  equina, 
and  then  the  posterior  root-zones  in  the  dorsal  region  are  implicated  in 
the  sclerosis  as  well  as  the  columns  of  Goll.  In  chronic  transverse 
myelitis  the  whole  thickness  of  the  spinal  cord  is  implicated  at  the  level 
of  the  chief  focus  of  disease,  and  at  this  point  the  cord  may  be  found 
softened.  Above  the  level  of  the  main  lesion  the  columns  of  Goll  and 
the  direct  cerebellar  tracts  undergo  an  ascending,  and  below  this  level 
the  lateral  columns  undergo  a  descending  sclerosis.  Evidences  of  a 
central  myelitis  are  also  frequently  observed,  the  motor  ganglion  cells 
are  completely  destroyed  immediately  above  and  below  the  main  focus, 
while  in  the  parts  which  are  remote  from  this  lesion  the  morbid  changes 
are  restricted  to  the  central  columns  and  the  accessory  nuclei.  In 
compression  myelitis  the  primary  disease  may  consist  of  caries,  cancer, 
or  some  other  disease  of  the  vertebral  column,  but  it  is  unnecessary  to 
describe  all  these  diseased  conditions  in  this  place.  It  may  also  consist 
of  some  forms  of  meningitis,  of  an  accumulation  of  pus  between  the 
dura  mater  and  vertebrae,  or  hematoma  of  the  spinal  dura  mater,  but 
these  aff'ections  will  subsequently  be  described.  The  following  peri- 
meningeal  and  meningeal  tumors  have  been  found  in  the  vertebral 
canal,  namely:  Lipoma,  originating  either  from  the  tissue  outside  the 
dura  mater  or  from  the  pia  mdiiev;  fibroma  ojid  fibrosarcoma,  vihxch. 


VARIETIES    OF    DIFFUSED    MYELITIS.  565 

may  be  situated  either  within  or  without  the  sac  of  the  dura  mater* 
sarcoma,  myxoma,  and  psammoma,  originating  from  the  pia  mater 
or  arachnoid  ;  enchondroma,  springing  from  the  vertebrae  and  dura 
mater;  osteoyna,  appearing  as  disks  in  the  arachnoid,  and  as  a  diffused 
ossification  of  the  dura  mater;  multiple  fibrous  melanoma,  exception- 
ally found  in  the  spinal  canal ;  carcinoma,  almost  always  met  with  as  a 
secondary  growth  from  the  mammae  or  vertebra;  miliary  tubercles, 
which  are  always  found  on  the  soft  membranes;  and  syphiloma,  which 
appears  as  gummata  of  the  dura  or  pia  mater.  Neuromata,  either 
true  or  false,  have  been  found  on  the  roots  of  the  spinal  nerves,  and 
are  most  frequently  situated  on  the  cauda  equina.  Parasitic  growths 
are  rarely  met  with  in  the  vertebral  canal,  but  echinococcus  has  been 
occasionally  met  with,  and  Westphal  has  reported  a  case  of  cysticercus" 
cellulos?e  of  the  spinal  cord. 

The  following  are  the  intramedullary  tumors  which  have  been  ob- 
served, namely:  Glioma,  which  may  form  a  rounded  tumor  or  may 
infiltrate  the  gray  matter  throughout  the  whole  length  of  the  spinal 
cord;  myxoglioma,  which  is  only  a  variety  of  glioma;  gliosarcoma, 
myxosarcoma,  sarcoma,  and  carcinoma  are  rare  in  the  substance  of  the 
cord;  nested  sarcoma,  with  calcareous  deposit  at  parts  of  the  growth 
forming  psammoma,  may  infiltrate  considerable  portions  of  the  cord 
and  replace  the  nervous  tissues  while  retaining  the  form  of  the  cord ; 
solitary  tubercles,  which  may  be  situated  either  in  the  gray  or  white 
matter;  syphilotna,  which  in  the  form  of  gumma  is  only  rarely  found 
in  the  substance  of  the  cord;  and  the  cystic  dilatation  described  as 
syringomyelitis. 

The  substance  of  the  spinal  cord  is  rendered  more  or  less  flat  and 
thin  at  the  point  compressed,  so  that  it  may  be  reduced  to  the  size  of  a 
small  quill,  and  in  chronic  cases  the  usual  ascending  and  descending 
changes  occur  above  and  below  the  level  of  the  lesion. 

In  hemiparaplegia  the  chief  lesion  and  the  secondary  changes  are 
restricted  to  one-half  of  the  cord.  Interruption,  with  subsequent  de- 
scending sclerosis  of  the  fibres  of  the  lateral  column,  produces  a  spas- 
modic paralysis  of  the  muscles,  vaso-motor  paralysis,  and  loss  of  the 
muscular  sensibility  and  the  muscular  sense  of  the  parts  innervated 
from  below  the  level  of  the  lesion,  while  destruction  of  the  posterior 
horns  and  the  posterior  columns,  causes  loss  of  the  sense  of  touch  and 
temperature,  and  of  common  sensation  on  the  side  opposite  the  lesion 
(Fig.  173).  The  anaesthetic  belt  which  surrounds  the  half  of  the  body 
on  a  level  with  and  on  the  same  side  as  the  lesion,  is  caused  by  impli- 
cation of  the  posterior  root-fibres,  and  the  narrow  hyperaesthetic  zone 
which  is  frequently  observed  on  both  sides  above  the  level  of  the  anses- 


566 


MYELITIS. 


thetic  belt,  is  supposed  by  Brown-Sequard  to  be  caused  by  irritation  of 
descending  fibres  of  those  posterior  roots  which  are  situated  immedi- 
ately above  the  level  of  the  lesion.  In  uiiiversal progressive  myelitis 
the  whole  of  the  transverse  area  of  the  cord  is  diseased  in  the  lumbar 
and  lower  dorsal  regions,  but  in  the  upper  dorsal  and  cervical  regions, 
the  sclerosis  may  be  limited  to  the  columns  of  Goll  and  the  direct  cere- 

FiG.  173. 

It      t  t      tl 


Diagram  of  the  Gouhse  of  the  Piunxipai.  (,'oxdu(-tino  Paths  within  the  f'oRD.  (After  Krb.) 
1  and  1',  The  motor  and  vaso-motor  tnicts,  passing  through  tlie  anterior  root  (i;),  and  remaining  on  the 
eame  side  of  the  cord  ;  2  and  2',  Tracts  which  conduct  the  muscular  sensibility,  also  passing  through  the 
anterior  roots,  and  remaining  on  the  same  side  of  the  cord:  3  ami  3',  The  tracts  which  conduct  sensory 
impressions  of  touch,  temperature,  pain,  and  tickling.  These  enter  flic  cord  through  the  posterior  roots, 
and  cross  to  the  other  side,  and  pursue  their  course  upwards  on  that  side.  Section  of  the  right  half  of  the 
cord  (n)  must  interrupt  conduction  through  the  motor,  vaso-motor,  and  musculo-sensory  tracts  (1  and  2) 
on  the  right  side,  and  the  cutaneous  sensory  tracts  on  the  left  side  (3'). 


bellar  tracts,  while  associated  with  them  may  sometimes  be  found  a 
certain  degree  of  chronic  central  myelitis. 

In  chronic  myelo-menim/itis  the  spinal  cord  is  surrounded  by  a  ring 
of  sclero.sed  tissue,  and  consequently  this  form  of  myelitis  has  been 
named  by  Yulpian  peripheric  or  cortical  myelitis,  or  ring-shaped  scle- 
rosis.    Chronic  disseminated  myelitis  will  be  subsequently  described. 

Treatment. — In  acute  myelitis  active  antiphlogistic  treatment  must 
be  adopted  during  the  febrile  stage  and  Chapman's  ice  bag  should  be 
applied  along  the  spine,  while  the  patient  should  lie  as  much  as  possible 
on  his  side  or  abdomen.  It  is  also  desirable  to  place  the  patient  on  a 
water  bed  and  the  parts  exposed  to  pressure  should  be  sponged  with 
brandy  or  whiskey,  and  dusted  with  an  absorbent  powder  in  order  to 
prevent,  if  possible,  the  formation  of  beds<ores.     In  the  very  acute  stage 


VARIETIES    OF    DIFFUSED    MYELITIS.  567 

of  myelitis  a  saline  mixture  may  be  given  in  order  to  maintain  the 
activity  of  the  skin  and  kidneys,  and  the  bowels  should  be  freely  acted 
on  by  mineral  waters  containing  sulphate  of  magnesia,  or  bv  senna 
rhubarb,  or  castor  oil.  Belladonna  and  ergot  are  supposed  to  contract 
the  capillaries  of  the  spinal  cord  and  either  one  or  other  may  be  ad- 
ministered in  the  early  stage  of  myelitis,  and  when  the  fever  has  sub- 
sided iodide  of  potassium  may  be  given  to  promote  absorption  of  effused 
products.  When  myelitis  is  developed  in  the  course  of  syphilis  large 
doses  of  iodide  of  potassium  should  be  administered,  while  mercury 
should  also  be  given  either  in  combination  with  the  iodide  salt,  by  in- 
unction, or  by  subcutaneous  injection.  Counter-irritation  and  electrical 
treatment  should  not  be  used  until  the  disease  has  become  more  or  less 
chronic.  Great  care  should  be  observed  in  introducing  the  catheter  for 
fear  of  setting  up  or  aggravating  cystitis,  and  every  precaution  should 
be  taken  to  prevent  the  introduction  of  bacteria  into  the  bladder  along 
with  the  instrument. 

Chronic  myelitis  must  be  treated  in  the  earlier  stages  of  the  disease 
on  the  same  general  principles  as  are  applicable  to  the  acute  disease. 
The  patient  should  be  kept  in  the  recumbent  posture,  the  usual  pre- 
cautions against  the  appearance  of  cystitis  and  bedsores  must  be  taken, 
and  ergot,  belladonna,  or  iodide  of  potassium  should  be  given  internally. 
Counter-irritation  to  the  vertebral  column  should  only  be  used  with 
caution,  but  in  transverse  myelitis  Corrigan's  button  may  be  applied 
at  two  or  three  points  on  each  side  of  the  vertebral  column  opposite  the 
seat  of  the  lesion.  The  application  of  a  water  douche  at  a  temperature 
of  from  98°  to  104°  F.  over  the  back  is  sometimes  very  soothing. 
When  all  acute  symptoms  have  sul;)sided  and  the  disease  is  more  or  less 
stationary  arsenic  or  phosphol'us  with  cod-liver  oil  may  be  found  useful, 
but  strychnine  should  on  no  account  be  administered. 

Baths  of  various  kinds  are  found  useful  in  the  treatment  of  chronic 
myelitis,  and  Erb  recommended  the  use  of  the  thermal  brine  baths  Avith 
a  temperature  of  from  88°  to  78°  F.,  while  ordinary  brine  baths, 
chalybeate,  and  mud  baths  are  recommended  by  others.  The  temper- 
ature in  most  cases  should  in  my  opinion  be  considerably  above  that 
recommended  by  Erb,  but  this  point  must  be  largely  determined  by  the 
feelings  of  the  patient. 

Hydropathic  treatment  is  also  useful,  but  great  care  should  lie  taken 
not  to  use  a  too  exciting  method,  and  consequently  cold  douches  and 
slappings  should  be  avoided. 

The  galvanic  current  is  one  of  the  most  useful  therapeutic  agents  for 
the  treatment  of  chronic  myelitis.  The  poles  should  be  placed  over  the 
vertebral  column  in  such  positions  that  the  diseased  portion  of  the  cord 


568  MYELITIS. 

is  included  in  the  circuit,  and  either  a  stabile  or  a  slowly  labile  current 
may  be  employed.  The  currents  should  not  be  strong  and  each  appli- 
cation should  be  of  short  duration.  This  treatment  should  be  continued 
for  months,  being  occasionally  interrupted  but  only  to  be  recommenced 
after  a  brief  pause. 

The  patient  should  avoid  all  overexertion,  or  mental  excitement,  and 
should  lead  a  very  regular  life,  Avhile  the  diet  should  be  simple,  nutritious, 
and  easy  of  digestion.  Alcoholic  drinks,  tea,  coffee,  and  tobacco  should 
only  be  used  very  sparingly,  and  sexual  intercourse  should  be  confined 
within  the  strictest  limits  or  absolutely  prohibited.  Residence  in  a 
mountainous  region  at  a  moderate  elevation,  or  at  the  seaside,  will  be 
useful,  and  it  is  often  advisable  for  the  patient  to  spend  the  winter  in 
the  South.  When  completely  paraplegic  the  patient  should  be  allowed 
to  enjoy  the  fresh  air  in  a  wheeled  chair,  and  when  bedridden  care 
should  be  taken  that  the  patient  is  made  to  lie  alternately  on  either  side 
or  in  the  prone  position  in  order  to  avoid  as  long  as  possible  the  forma- 
tion of  bedsores,  the  appearance  of  which  would  be  accelerated  were 
the  patient  permitted  to  be  always  in  the  recumbent  posture. 

Pain  must  be  relieved  by  narcotics,  such  as  the  subcutaneous  injection 
of  morphia.  The  faradic  brush,  Preissnitz's  compresses,  applications  of 
chloroform,  and  frictions  with  veratrine  ointment  and  soothing  liniments 
will  be  found  useful  in  the  treatment  of  many  of  the  sensory  disorders 
which  arise  in  the  course  of  a  chronic  myelitis,  while  electrical  currents 
form  the  best  local  application  for  the  removal  of  the  paralyses,  atrophies, 
and  anaesthesia  which  persist  after  the  disease  has  run  it  course. 


CHAPTEK    XII. 

DISEASES  OF  THE  SPINAL  MEMBRANES. 
I.  VASCULAR   DISEASES   OF   THE   SPINAL   MEMBRANES. 

1.  Hypek^mia. 

Hyperj^.mia  of  the  spinal  membranes  has  already  been  considered 
along  with  hyperpemia  of  the  spinal  cord. 

2.    H.EMATORRIIACHIS    (MENINGEAL    ApOPLEXY). 

Etiology. — Very  little  is  known  with  regard  to  the  predisposing  causes 
of  hsematorrhachis,  but  it  occurs  more  frequently  in  men  than  in  women. 
The  most  usual  exciting  causes  are  injuries  of  the  spinal  column,  caries 
of  the  vertebrfe,  excessive  bodily  exertion,  the  spasms  of  convulsive 
diseases  like  epilepsy,  and  the  sudden  suppression  of  accustomed  dis- 
charges. It  may  also  occur  in  such  diseases  as  scorbutus,  purpura 
hemorrhagica,  smallpox,  typhoid  fever,  and  other  acute  infectious  diseases. 
Aneurisms  have  been  known  to  rupture  into  the  vertebral  canal,  and 
blood  effused  into  the  l^rain  or  cerebral  membranes  may  sometimes  pass 
down  into  the  spinal  canal. 

Symptoms. — The  patient  is  suddenly  attacked  with  violent  pains  and 
falls  down,  but  generally  without  loss  of  consciousness.  The  severest 
pain  is  localized  at  a  spot  over  the  spinal  column  corresponding  to  the 
seat  of  the  hemorrhage,  but  this  pain  is  associated  with  eccentric  sensa- 
tions such  as  formication,  burning,  and  tingling,  which  radiate  along  the 
distribution  of  the  nerves  the  roots  of  which  are  first  implicated,  while 
an  objective  examination  reveals  anaesthesia  or  hypersesthesia  of  these 
nerve-territories.  The  early  motor  symptoms  consist  of  spasmodic 
jerking  and  trembling  of  the  extremities,  or  of  a  tonic  spasm  of  various 
groups  of  muscles  which  causes  the  extremities  to  be  forcibly  flexed  or 
the  head  to  be  retracted  or  rotated  towards  one  shoulder.  The  vertebral 
column  is  likewise  stiff"  and  painful  and  the  patient  is  unable  to  raise 
himself  in  bed  or  to  assume  the  sitting  posture. 

The  irritative  symptoms  give  place  after  a  time  to  those  of  sensory 
and  motor  paralysis,  but  complete  paraplegia  is  rare,  and  the  anaesthesia 


570  DISEASES    OF    THE    SPINAL    MEMBKAXES. 

also  is  seldom  complete  on  objective  examination,  but  the  patient  com- 
plains of  subjective  sensations  of  SAvelliug  and  heaviness  of  the  limbs 
and  trunk,  and  of  feelings  of  numbness  and  tingling. 

The  reflex  excitability  is  said  to  be  depressed  in  some  cases,  but 
probably  this  only  occurs  in  the  region  supplied  by  fibres  derived  from 
the  nerve  roots  directly  aifected ;  weakness  of  the  bladder  and  rectum 
is  present  only  in  severe  cases,  and  fever  is  absent  at  first,  but  may 
occur  on  the  second  or  third  day.  The  symptoms  remain  stationary 
for  some  time,  but  Avhen  the  disease  is  uncomplicated  it  often  runs  a 
favorable  course  and  a  tolerable  recovery  may  take  place  in  a  few  Aveeks 
or  months. 

Varieties. — (1)  If  the  lumbar  region  is  affected  there  are  pains  and 
stiffness  in  the  loins,  tearing  pains  in  the  loAver  extremities,  perineum, 
bladder,  and  genitals,  well-marked  paralysis  of  the  lower  extremities, 
loss  of  the  reflexes,  and  paralysis  of  the  bladder  and  rectum. 

(2)  If  the  dorsal  region  is  affected  there  are  pains  in  the  back  and 
abdomen,  girdle-pain,  stiffness  in  the  dorsal  part  of  the  spine,  paralysis 
of  the  legs  and  abdominal  muscles,  and  retention  of  the  reflexes  in  the 
lower  extremities. 

(3)  If  the  cervical  region  is  affected  there  are  pains  in  the  arms  and 
shoulders,  stiffness  of  the  neck,  and  pain  in  the  occiput.  The  anaes- 
thesia and  paralysis  are  most  marked  in  the  upper  extremities,  and 
oculo-pupillary  symptoms,  difficulty  of  breathing,  and  a  retarded  and 
feeble  pulse  may  be  present.  When  the  upper  cervical  region  is  affected 
sudden  death  from  respiratory  paralysis  may  occur. 


II.   INFLAMMATION    OF    THE  SPINAL    DURA    MATER 
(PACHYMENINGITIS  SPINALIS,  PERIMENINGITIS). 

Pachymeningitis  may  be  divided  into  inflammation  of  1,  the  external 
layers  of  the  dura  mater  and  the  surrounding  cellular  tissue,  or  external 
pachymeningitis ;  and  2,  the  internal  surface  of  the  membrane  with 
deposition  of  morbid  products  between  the  dura  mater  and  arachnoid, 
or  internal  piachy meningitis. 

1.  Pachymexingitis  Spinalis  Externa  (Peripachymeningitis). 

Etiology. — Various  diseases  in  and  about  the  vertebral  column,  such 
as  vertebral  caries  and  bedsores,  constitute  the  most  fre(j[uent  causes  of 
this  disease,  but  it  may  possibly  arise  occasionally  as  an  idiopathic 
affection. 


1 


INFLAMMATION    OF    THE    SPINAL    DURA    MATER.      571 

Symptoms. — The  symptoms  of  external  spinal  pachymeningitis  may 
develop  in  an  acute  or  chronic  form.  In  the  acute  purulent  forms  the 
prominent  symptoms  are  caused  by  irritation  and  consist  of  pain  and 
rigidity  of  the  back,  great  tenderness  on  pressure,  shooting  pains  in  the 
lower  extremities,  and  pain  in  the  joints,  while  there  may  he  consider- 
able elevation  of  temperature,  diarrhoea,  and  other  general  symptoms. 
In  the  acute  form  the  sym])toms  of  transverse  myelitis  may  be  more  or 
less  suddenly  developed.  In  the  chronic  fibrinous  form  of  the  disease 
the  premonitory  symptoms  are  obscure  and  the  symptoms  of  slow  com- 
pression of  the  cord  or  of  a  chronic  transverse  myelitis  with  secondary 
degenerations  predominate.  These  symptoms  comprise  both  sensory 
and  motor  paralysis  below  the  level  of  the  lesion,  muscular  tension, 
increased  cutaneous  reflexes  and  tendon-reactions,  and  after  a  time 
paralysis  of  the  sphincters  and  bedsores. 


2.  Pachymeningitis  Interna. 

Internal  pachymeningitis  may  be  divided  into  a,  the  hypertrophic, 
and  h,  the  hemorrhagic  varieties. 

a.  Pachymeningitis  Interna  Hypertrophica. 

Etiology. — The  causes  usually  assigned  to  the  hypertrophic  variety 
are  exposure  to  cold  and  damp,  and  the  excessive  use  of  alcohol. 

Symptoms. — The  hypertrophic  form  usually  occurs  in  the  cervical 
region  and  it  generally  begins  by  neuralgiform  pains  in  the  neck  and  head 
which  shoot  into  the  shoulders  and  arms,  and  by  a  painful  girdle  sensa- 
tion in  the  upper  part  of  the  chest.  The  muscles  of  the  neck  are  in 
a  state  of  spasmodic  rigidity,  the  patient  often  complains  of  formication 
and  numbness  of  the  upper  extremities,  and  vesicular  herpetic  eruptions 
may  make  their  appearance  on  the  upper  extremities. 

The  transition  to  the  second  stage  is  characterized  by  the  gradual 
development  of  paralysis,  which  is  usually  of  the  atrophic  variety  in 
the  upper  extremities,  and  of  the  spasmodic  in  the  lower.  When  the 
lesion  is  situated  on  a  level  with  the  eighth  cervical  and  first  dorsal 
nerves,  both  hands  are  maintained  in  the  position  of  exaggerated  ex- 
tension, and  the  segments  of  the  thumb  are  also  extended,  while  the 
phalanges  of  the  fingers  are  partially  flexed  on  the  metacarpal  bones 
and  upon  one  another,  the  fingers  being  thus  held  like  claAvs  (Fig.  175). 
In  a  case  o^ pachymeningitis  on  the  level  of  the  eighth  cervical  and  first 
and  second  dorsal  nerves  which  was  under  my  care,  the  hands  were 
only  hyperextended  when  the  patient  endeavored  to  grasp,  while  the 


572 


DISEASES    OF    THE    SPINAL    MEMBEANES. 


distribution  of  the  anaesthesia  is  seen  in  Fig.  174.  Oculo-pupillary 
phenomena,  first  of  the  irritative  kind,  and  as  the  disease  advances  of 
the  paralytic  kind,  are  always  present  Avhen  the  eighth  cervical  and 
first  dorsal  nerve  roots  are  implicated,  and  they  may  also  be  present 
when  the  lesion  is  situated  on  a  higher  level  if  the  cord  undergoes 
considerable  compression,  or  if  there  be  transverse  myelitis.  When 
the  lesion  is  situated  above  the  level  of  the   eighth   cervical  nerve  the 

Fig.  174. 


distended  position  of  the  hand,  and  the  distribution  of  the  anaesthesia 
differ  from  those  just  described.  In  a  case  under  the  care  of  my  col- 
league, Dr.  Leach,  in  which  the  lesion  was  situated  on  a  level  with  the 
fifth,  sixth,  and  probably  the  seventh  cervical  nerves,  the  arm  was  held 
close  to  the  side,  the  forearm  was  extended  on  the  arm  and  strongly 
pronated,  the  hand  was  strongly  flexed  on  the  arm,  the  fingers  were  on 
a  line  with  or  only  slightly  extended  on  the  metacarpal  bones,  and  the 
phalanges  were  extended  upon  one  another,  while  the  thumb  was  flexed 
into  the  palm.     All  the  muscles  of  the  forearm  and  hand  were  doubt- 


INFLAMMATION    OF    THE    SPINAL    DURA    MATKR.      573 

less  more  or  less  paralyzed,  but  the  muscles  supplied  by  tlie  musculo- 
spiral  nerve  were,  on  the  whole,  more  aftected  than  those  supplied  by 
the  ulnar  and  median  nerves,  contrary  to  what  takes  place  when  the 
lesion  is  situated  on  a  level  with  the  junction  of  the  cervical  and  dorsal 
regions  of  the  cord.  In  another  case  under  my  care,  in  which  the 
spinous  process  of  the  fourth  cervical  vertebra  was  tender  to  pressure 
and  the  skin  of  that  region  sensitive  to  the  cathode  of  the  galvanic 
current,  the  symptoms  were  slight  spasmodic  paralysis  of  the  lower 
extremities;  feebleness  with  diffused  wasting  of  all  the  muscles  of  the 

Fig.  175. 


Attitude  of  the  Hand  in  Pachymeningitis  Cekvicalis  HypERTRorHirA,  when  the  Lesion  is 

SITUATED   ON   A   LeVEI,   WITH   THE    UPPER   HALF   OF   THE   CERVICAL    ENLARGEMENT. 

upper  extremities,  most  marked  in  the  deltoid,  biceps,  and  supinator 
longus;  arthropathies  of  the  small  joints  of  both  hands;  dilatation  of 
the  pupils,  with  widening  of  the  palpebral  apertures,  most  pronounced 
on  the  left  side;  and  troublesome  hiccough,  which  persisted  continuously 
during  waking  hours  for  about  ten  days  after  the  patient  was  laid  on 
her  back  in  bed,  and  which,  after  abating,  could  be  readily  excited 
again  by  any  movement  of  the  head.  The  sensory  phenomena  con- 
sisted of  stiff"ness  of  the  neck,  and  pains  on  a  level  with  the  fourth 
cervical  vertebra,  which  radiated  on  both  sides  of  the  neck  and  down 
the  shoulders,  but  there  was  no  anaesthesia.      The  patient  recovered. 


h.  Pachymeningitis  Interna  Hemorrliagica. 

The  symptoms  of  internal  hemorrhagic  pachymeningitis  are  very 
obscure,  and  are  usually  complicated  with  those  of  coexisting  cerebral 
disease.  They  consist  of  pains  in  the  loins  and  back,  tearing  pains  in 
the  extremities,  stiffness  of  the  vertebral  column,  increasing  muscular 


574  DISEASES    OF    THE    SPINAL    MEMBRANES. 

weakness  which  may  gradually  develop  into  complete  paraplegia  with 
contractures,  various  degrees  of  cutaneous  hyperpesthesia  or  anaesthesia, 
and  weakness  of  the  bladder.  If  a  patient  with  these  symptoms  is  at 
the  same  time  suffering  from  chronic  alcoholism  and  cerebral  paralysis, 
internal  hemorrhagic  pachymeningitis  may  be  suspected. 


III.  INFLAMMATION  OF  THE  SPINAL  PIA  MATER  AND  ARACH- 
NOID—LEPTOMENINGITIS  SPINALIS  ;  PERIMYELITIS  AND 
ARACHNITIS. 

Spinal  leptomeningitis  presents  many  varieties,  but  for  practical 
purposes  it  will  suffice  to  divide  the  disease  into  the  acute  and  the 
chronic  forms. 

1.  Leptomeningitis  Spinalis  Acuta. 

Etiology. — The  predisposing  causes  of  acute  meningitis  are  a  scrofu- 
lous or  tubercular  constitution,  insufficient  food,  damp  dwellings,  and 
sexual  or  other  excesses.  The  disease  attacks  by  preference  children, 
young  persons,  and  the  male  sex.  The  most  important  of  the  exciting 
causes  are  exposure  to  cold,  wounds  and  injuries  of  the  vertebral  column, 
and  extension  of  inflammation  from  neighboring  structures.  Spinal 
meningitis  may  occur  along  with  or  during  convalescence  from  pneu- 
monia, acute  articular  rheumatism,  and  febrile  and  infectious  diseases, 
and  it  is  a  very  usual  complication  of  tul)ercular  basal  meningitis. 
Epidemic  cerebro-spinal  meningitis  is  an  infectious  disease,  and  its 
consideration  is  beyond  the  scope  of  this  work. 

Symptoms. — Acute  spinal  meningitis  is  generally  complicated  by  a 
simultaneous  affection  of  the  cerebral  pia  mater,  and  it  is  not  always 
easy  to  separate  the  spinal  from  the  cerebral  symptoms.  The  outbreak 
of  the  characteristic  symj)toms  of  si)inal  meningitis  may  be  preceded 
by  premonitory  symptoms  consisting  of  general  heaviness  and  depres- 
sion, slight  chilliness,  gastric  disturbances,  transitory  pains  in  the  head 
and  back,  restlessness,  and  sleeplessness.  'I'he  characteristic  symptoms 
of  the  disease  are  ushered  in  by  a  rigor  followed  by  fever  of  irregular 
type,  and,  if  the  pia  mater  of  the  brain  be  affected,  vomiting  and  other 
severe  cerebral  symptoms  are  present.  The  patient  now  complains  of 
an  intense,  deep-seated,  boring  pain  in  the  loins,  back,  or  nape  of  the 
neck,  corresponding  to  the  seat  of  the  lesion.  The  pain  radiates  from 
the  vertebral  column  round  the  trunk,  and  shoots  in  all  directions 
through  the  extremities,  while  it  is  aggravated  by  all  movements  of  the 
spine,  and  by  pressure  on  the  spinous  processes.  It  may  abate  for  a 
time,  but  a  remission  is  generally  folloAved  by  an  exacerbation  of  great 
severity. 


INFLAMMATION    OF    SPINAL    PIA     MATER.  575 

The  muscles  of  the  back  are  in  a  state  of  spasmodic  rigidity,  which 
may  sometimes  extend  the  whole  length  of  the  spine  so  as  to  resemble 
a  tetanic  seizure,  but  at  other  times  is  limited  to  a  part  of  the  vertebral 
column  corresponding  to  the  seat  of  the  lesion.  The  muscles  of  the 
extremities  are  also  tense  and  contracted,  and  the  limbs  are  then  rigid 
and  immovable  or  the  subjects  of  painful  twitchings. 

Cutaneous  and  muscular  hyperesthesia  are  often  present  in  the  ex- 
tremities and  trunk,  the  distribution  corresponding  to  the  areas  supplied 
by  fibres  derived  from  the  posterior  roots  of  the  part  affected.  The 
reflex  actions  are  increased  at  first,  but  they  are  liable  to  be  diminished 
or  lost  in  the  later  stages  of  the  lesion. 

Disorders  of  the  function  of  the  bladder  occur  at  an  early  period  of 
the  disease,  caused,  most  probably,  by  spasm  of  the  sphincters,  and 
when  the  cervical  region  is  affected  the  respiratory  muscles  become 
rigid  and  painful,  giving  rise  to  a  difficulty  of  breathing,  which  may 
increase  to  such  an  extent  as  to  cause  asphyxia. 

As  the  disease  progresses  cutaneous  sensibility  becomes  diminislied 
and  complete  anaesthesia  may  be  established,  while  the  extremities 
manifest  various  degrees  of  motor  weakness  up  to  complete  paralysis. 
The  pupils  may  be  contracted,  dilated,  or  unequal,  and  if  the  inflam- 
mation extends  to  the  medulla  oblongata  or  to  the  base  of  the  cranium, 
the  patient  suffers  from  vertigo,  headache,  paralysis  of  ocular  muscles, 
and  delirium,  which  soon  terminates  in  unconsciousness  and  fatal  coma 
with  hyperpyrexia.  At  other  times  deceitful  signs  of  temporary  im- 
provement appear,  but  paralysis  and  bedsores  supervene,  and  the 
patient  dies  from  septic  fever.  In  slight  cases  recovery  may  take 
place,  but  convalescence  is  slowly  established,  and  the  symptoms  of 
sensory  and  motor  irritation  disappear  only  after  a  long  period.  In 
many  cases  incurable  defects  are  left  behind,  consisting  of  anaesthesia, 
some  degree  of  ataxia,  atrophic  paralysis  of  some  groups  of  muscles, 
and  spasmodic  paralysis  of  other  gi-oups. 


2.  Leptomeningitis^  Spinalis  Chronica. 

Etiology. — The  disease  frequently  develops  from  the  acute  form  and 
is  produced  from  the  same  causes. 

Symptoms. — The  disease  begins  more  insidiously  than  the  acute 
variety.  The  patient  complains  of  a  gradually  increasing  pain  and 
stiffness  in  the  back,  various  parajsthesiae  in  the  lower  extremities,  and 
a  feeling  of  weakness  and  heaviness  of  the  limbs.  Eccentric  pains 
are  felt  in  the  areas  of  distribution  of  the  nerves  Avhose  roots  are  impli- 


576  DISEASES    OF    THE    SPINAL    MEMBRANES. 

cated  in  the  lesion,  consisting  of  shooting  pains  in  the  lower  or  upper 
extremities  or  a  girdle  sensation  round  the  body  according  to  the  situation 
of  the  lesion.  Hypersesthesia  of  the  skin  of  the  lower  extremities  is 
frequently  present,  but  anaesthesia  is  rare,  and  when  present  it  consists 
mostly  of  blunting  of  the  sensibility  of  the  feet  and  lower  part  of  the 
legs.  The  motor  symptoms  consist  of  stiffness  of  the  back  and  neck, 
and  an  involuntary  drawing  up  or  extension  of  the  extremities,  but  the 
phenomena  of  motor  irritation  are  never  very  prominent  in  this  disease. 
After  a  time  the  limbs  become  heavy  and  feeble,  but  complete  paraplegia 
is  rare.  When,  however,  the  lower  extremities  are  more  or  less  com- 
pletely paralyzed  the  muscles  become  tense,  and  contractures  with  flexion 
of  the  limbs  or  flexion  of  one  limb  and  extension  of  the  other  are  estab- 
lished, but  the  patellar  tendon-reactions  are  often  absent  under  such 
circumstances.  If  there  be  a  considerable  effusion  of  spinal  fluid,  the 
paralysis  becomes  augmented  when  the  patient  stands,  but  at  other  times 
it  is  most  marked  when  the  patient  is  lying  on  his  back,  probably  because 
the  cord  becomes  passively  congested.  In  severe  cases  the  paralyzed 
muscles  may  undergo  atrophy  ;  aniesthesia  is  developed  ;  the  cutaneous 
reflexes  and  the  tendon-reactions  are  lost ;  bedsores  and  cystitis  appear 
and  the  patient  dies  from  pyaemia. 

Morbid  Physiology. — The  morbid  anatomy  of  hemorrhage  and  in- 
flammation of  the  spinal  membranes  has  already  been  sufiiciently  con- 
sidered. In  connecting  the  morbid  process  with  the  symptoms  the 
chief  points  to  notice  are  that  the  most  j)rominent  pheiiomena  of  the 
various  affections  are  caused  by  irritation  or  paralysis  of  the  posterior 
and  anterior  loots  on  a  level  with  the  lesion,  and  irritation  or  paralysis 
of  the  sensory  and  motor  conducting  paths  below  the  level  of  the  lesion. 
In  disease  of  the  membranes  tliere  are  two  causes  of  sensory  disorder — 
disease  of  the  posterior  roots  and  of  the  conducting  paths  in  the  posterior 
columns  and  posterior  gray  horns  ;  and  two  causes  of  spasm  or  paralysis 
— disease  of  the  anterior  roots  and  of  the  motor  conducting  paths  in 
the  lateral  columns.  It  is  important  to  remember  that  disease  of  the 
anterior  root  gives  rise  to  an  atrophic,  and  of  the  lateral  column  to  a 
spasmodic  paralysis.  In  cases  recovering  from  an  attack  of  meningitis 
ataxic  symptoms  may  be  present  from  the  persistence  of  the  disease  in 
the  posterior  columns,  and  when  the  posterior  columns  are  affected  on 
a  level  with  the  upper  part  of  the  lumbar  enlargement  the  patellar 
tendon-reactions  will  be  absent  from  interference  with  its  reflex  loop, 
whether  paralysis  be  present  or  not.  When  the  lesion  is  on  a  level 
with  the  cilio-spinal  region,  oculo-pupillary  symptoms,  and  when  on  a 
level  with  the  upper  part  of  the  lumbar  enlargement,  disorders  of  the 
hladder  and  rectum  will  be  present. 


INFLAMMATIOX    OF    SPINAL    PIA    MATEE.  577 

Treatment. — In  meningeal  hemorrhage  the  patient  should  be  main- 
tained at  rest  on  his  side  or  face  and  an  ice  bag  applied  to  the  vertebral 
column,  and  ergot  may  be  given  internally.  Leyden  recommends  the 
use  of  mercurial  inunction  and  repeated  small  doses  of  calomel  during 
the  period  of  reaction,  but  when  this  stage  has  passed  absorption  may  be 
promoted  by  the  administration  of  iodide  of  potassium.  The  vertebral 
column  may  be  painted  with  iodine,  and  the  galvanic  current  will  also 
be  found  useful  in  promoting  recovery. 

In  external  pachymeningitis  the  treatment  must  be  directed  ao-ainst 
the  primary  lesion,  and  when  vertebral  caries  is  present  the  patient  ought 
to  be  placed  on  his  back  on  a  water  bed  until  the  acute  symptoms  have 
subsided,  and  the  subsequent  treatment  must  be  conducted  with  a  Sayre's 
jacket  or  other  form  of  spinal  support.  The  actual  cautery  applied  in 
the  vicinity  of  the  diseased  vertebrae  is  often  a  very  useful  remedy,  and 
iodide  of  potassium,  iodide  of  iron,  or  friction  with  mercurial  ointment 
may  each  be  advantageously  employed  according  to  the  nature  of  the 
case.  When  the  primary  disease  has  been  arrested  and  the  symptoms 
have  become  chronic,  galvanic  treatment  Avill  be  found  to  promote  re- 
covery from  the  sensory  and  motor  disorders. 

In  internal  pachymeningitis  and  leptomeningitis  the  same  general 
principles  are  applied  to  the  treatment  of  both  diseases.  In  the  early 
stage  of  acute  meningitis  cold  must  be  applied  to  the  spine  by  means  of 
Chapman's  ice  bag,  while  leeches  may  be  applied  to  the  vertebral 
column  and  a  smart  saline  purgative  administered.  When  the  temper- 
ature has  fallen  blisters  or  some  other  form  of  counter-irritation  should 
be  applied  along  the  spine,  and  when  the  acute  symptoms  have  subsided 
a  mercurial  treatment  Avill  prove  useful,  inunction  being  probably  the 
most  efficient  method  of  administration.  The  patient  should  lie  on  his 
face  or  side,  and  when  hyperaesthesia,  pain,  or  sleeplessness  are  urgent 
symptoms  sedatives  must  be  given,  the  best  form  of  administration  being 
a  subcutaneous  injection  of  morphia.  Warm  baths  afford  great  relief, 
and  moist  packing  of  the  whole  body  often  soothes  and  induces  sleep. 

In  chronic  spinal  meningitis  repeated  blisters  may  be  applied  along 
the  vertebral  column,  while  moderate  doses  of  iodide  of  potassium  are 
given  internally.  Mercury  should  not  be  administered  unless  the 
presence  of  syphilis  is  suspected,  while  ergot  and  belladonna  have  not 
been  found  so  useful  as  in  myelitis.  Warm  baths  and  douches  are  very 
soothing  to  the  patient,  and  a  galvanic  current  of  moderate  strength 
may  be  employed,  either  applied  to  the  spine  or  in  tlie  course  of  the 
nerves  which  are  the  subjects  of  eccentric  pains. 


CHAPTEE    XIII. 

CERTAIN  FUNCTIONAL  DISEASES  OF  THE  NERVOUS  SYSTEM. 
I.  SPINAL  IRRITATION. 

Etiology. — The  female  sex  predispose  to  this  disease,  although  men 
are  occasionally  affected.  The  members  of  neuropathic  families  are 
o-enerally  attacked,  and  most  of  the  cases  occur  between  fifteen  and 
thirty  years  of  age. 

The  exciting  causes  are  emotional  disturbances,  sexual  excesses, 
exhausting  diseases,  and  everything  which  weakens  the  nervous  system. 

Symptoms. — The  symptoms  begin  with  headache,  sleeplessness,  in- 
creased nervous  irritability,  ill-defined  pains  in  the  back,  neuralgiform 
pains  in  the  face  or  extremities,  and  general  feebleness,  these  symptoms 
gradually  increasing  in  intensity  until  the  disease  is  fully  developed. 

The  patient  now  complains  of  pain  in  the  back,  which  is  aggravated 
by  exertion,  and  is  situated  most  frequently  between  the  shoulder- 
blades,  or  in  the  back  of  the  neck,  and  less  frequently  in  the  loins. 
The  spinous  processes  of  some  of  the  vertebmc  are  excessively  tender 
to  pressure,  and  over  these  processes  the  surface  is  found  to  be  very 
sensitive  when  a  hot  sponge  or  the  cathode  of  a  galvanic  current  is 
applied.  Tenderness  of  the  vertebrpe  to  pressure  is,  indeed,  the  most 
constant  and  important  symptom  of  spinal  irritation,  and  this  sign  is 
rendered  all  the  more  valuable  from  the  fact  that  spinal  tenderness  is 
never  a  prominent  symptom  of  myelitis  and  other  organic  diseases  of 
the  cord. 

The  patient  complains  of  various  parsesthesiae  and  neuralgiform  pains 
in  the  upper  and  lower  extremities,  occiput,  face,  pelvic  region,  bladder, 
genitals,  or  viscera ;  the  slightest  exertion  occasions  great  fatigue  and 
exhaustion ;  and  walking  soon  becomes  impossible  owing  to  the  exces- 
sive pain  caused  by  it. 

The  motor  symptoms  consist  of  fibrillary  twitchings,  spasms  of  some 
muscles,  choreic  movements,  hiccough,  and  even  permanent  contrac- 
tures in  rare  cases.  Epileptic  attacks  ai'e  said  to  have  been  occasionally 
observed,  but  it  is  more  likely  that  these  general  convulsions  were 
Ijysterical  seizures.  A  certain  degree  of  muscular  weakness  may  be 
present  in  some  cases,  but  real  paralysis  has  never  been  observed. 


NEUKASTHEXIA.  579 

The  vaso-motor  disorders  consist  of  coldness  of  the  hands  and  feet 
and  the  patients  are  apt  to  turn  pale  or  red  on  the  slightest  provocation. 

The  most  common  visceral  disorders  met  with  are  eructations,  nausea, 
vomiting,  palpitations,  asthmatic  breathing,  cough,  vesical  spasm,  and 
polyuria.  The  patient  also  complains  of  noises  in  the  ears,  dizziness, 
muscae  volitantes  and  other  disorders  of  vision,  sleeplessness,  and  great 
mental  depression  or  irritability.  The  brothers  Griffin  divided  the 
disease  into  several  varieties,  and  endeavored  to  connect  the  symptoms 
present  in  each  case  with  the  localization  of  the  spinal  tenderness  in 
the  cervical,  dorsal,  or  lumbar  regions,  but  the  symptoms  first  enumer- 
ated are  frequently  met  with  in  cases  of  hysteria  in  the  entire  absence 
of  spinal  tenderness.  I  have  never  been  able  to  assure  myself  that 
the  divisions  of  the  brothers  Griffin  are  borne  out  by  clinical  facts. 
Spinal  irritation  is  never  a  fatal  disease,  although  it  may  last  for  months 
or  years  and  cause  great  suffering  to  the  patient. 


II.  NEUKASTHENIA. 

Etiology. — Neurasthenia  consists  of  exhaustion  of  the  cerebro-spinal 
centres,  and  generally  occurs  in  neuropathic  families,  and  the  male  is 
more  liable  to  the  disease  than  the  female  sex.  Neurasthenia  may  be 
a  sequel  of  any  exhausting  disease,  but  it  is  generally  caused  by  over- 
work and  worry,  or  by  sexual  and  other  excesses. 

Symjjtoms. — The  symptoms  vary  according  as  the  weakness  declares 
itself  in  the  spinal  or  cerebral  centres,  although  in  most  cases  both 
groups  of  symptoms  are  variously  combined. 

In  spinal  neurasthenia  the  patient  complains  of  weakness  of  the 
lower  extremities,  which  may  sometimes  be  so  great  as  to  amount  to  a 
slight  degree  of  paralysis.  The  arms  also  are  readily  fatigued,  but 
the  weakness  in  them  never  reaches  the  same  degree  of  intensity  as  in 
the  legs.  The  sensory  disturbances  consist  of  pains  in  the  back  and 
neuralgiform  pains  in  the  extremities,  which  may  sometimes  be  so 
intense  as  to  simulate  the  pains  of  locomotor  ataxia,  although  in  the 
former  disease  they  are  never  so  acute  and  darting  as  in  the  latter. 
The  patient  also  complains  of  numbness  and  formication  in  the  lower 
extremities,  the  hands  and  feet  are  cold,  and  the  body  is  apt  to  be 
bathed  in  sweat  at  night,  and  during  the  day  on  slight  exertion.  The 
sexual  power  is  generally  diminished,  and  the  act  of  coition  is  followed 
by  great  prostration,  disturbed  sleep,  and  a  fidgetty,  restless  feeling  in 
the  lower  extremities.  The  functions  of  the  bladder  are  usually  normal, 
although  a  little  dribbling  of  urine  may  occasionally  be  present. 


580      FUNCTIONAL    DISEASES    OF    THE    NERVOUS    SYSTEM. 

In  cerebral  neurasthenia  one  of  the  most  constant  symptoms  is  a  dif- 
fused tenderness  of  the  scalp,  which  is  exquisitely  sensitive  to  a  slight 
touch,  such  as  that  caused  hy  a  comb  or  by  a  slight  ruffling  of  the  hair 
over  the  part,  but  the  pain  is  relieved  by  deep  and  steady  pressure. 
The  patient  also  complains  of  a  sense  of  pressure  over  the  vertex,  Avhich 
is  sometimes  compared  to  the  feeling  that  might  be  caused  by  a  mailed 
hand  being  laid  heavily  over  the  head.  This  pain,  which  is  distinct 
from  the  sense  of  tenderness,  is  most  proba,bly  caused  by  the  ani^emia 
which  so  frequently  accompanies  the  affection.  Neurasthenic  patients 
are  also  liable  to  suffer  from  migraine  headaches,  and  facial  neuralgia, 
but  the  only  connection  between  it  and  these  affections  appears  to  be 
that  all  of  them  are  liable  to  occur  in  neuropathic  families. 

The  motor  disorders  of  cerebral  neurasthenia  are  jerkings  of  the 
limbs,  which  are  particularly  troublesome  when  the  patient  is  about  to 
fall  asleep ;  tremors  of  the  hand ;  and  slight  clonic  spasms  of  the  facial 
muscles,  which  may  be  limited  to  the  orbicular  muscle  of  the  eye,  or 
to  the  angle  of  the  mouth,  or  implicate  a  large  number  of  the  muscles, 
so  as  to  constitute  a  decided  facial  tic.  The  patient  complains  of  heavi- 
ness of  the  limbs  and  is  soon  fatigued,  and  decided  paralysis  is  common 
in  females  but  not  in  males.  The  sensory  disorders  are  very  numerous 
in  cerebral  neurasthenia.  In  addition  to  the  sensory  disorders  already 
described  as  belonging  to  the  spinal  disease,  patients  are  liable  to  suffer 
from  numbness  and  tingling  in  the  extremities  from  slight  pressure  on 
the  nerves. 

Pressure  by  the  edge  of  a  chair  over  the  sciatic  nerve  causes  numb- 
ness of  the  foot,  while  tingling  of  the  hand  is  readily  caused  if  the 
arm  rests  for  a  short  time  over  a  chair.  Sleep  is  frequently  disturbed 
by  feelings  of  "  pins  and  needles  "  in  one  hand  and  arm,  caused  doubt- 
less by  a  slight  pressure  exerted  on  the  brachial  plexus  or  some  of  its 
branches.  Hemiansesthesia  is  a  common  symptom  of  neurasthenia  in 
women,  and  men  sometimes  complain  of  abnormal  sensations  in  one- 
half  the  body  but  in  them  they  usually  assume  the  form  of  a  hyper- 
algesia rather  than  loss  of  feeling.  Tlie  nerves  of  special  sense  are 
almost  always  affected.  The  patient  complains  of  a  sour  or  bitter  taste, 
and  may  have  subjective  sensations  of  the  smell  of  phosphorus  or  other 
odors,  while  his  perception  of  flavors  and  relishes  is  much  diminished. 

The  patient  is  also  troubled  with  various  noises  in  the  ears,  and  on 
lying  down  at  night  he  is  so  much  disturbed  with  rushing  sounds  and 
hearing  the  beating  of  his  heart  with  unusual  distinctness  that  he  is 
obliged  to  lie  on  his  back  to  avoid  his  ear  coming  in  contact  with  the 
pillows,  while  in  the  morning  there  is  decided  deafness  which  is  accom- 
panied by  distressing  attacks  of  yawning.     Sight  is  affected  in  various 


NEURASTHENIA.  581 

ways ;  the  patient  suffers  from  muscae  volitantes,  colored  vision,  and 
spectral  illusions,  the  latter  being  specially  liable  to  appear  when  the 
eyes  are  closed  for  sleep  at  night.  Vision  may  be  impaired  either  from 
defective  nutrition  of  the  sensory  nervous  mechanism,  or  from  feebleness 
of  accommodation  and  of  the  internal  recti  muscles. 

The  vaso-motor  disorders  of  neurasthenia  are  numerous.  One  of  the 
most  common  is  blushing,  which  may  spread  not  only  over  the  face,  but 
also  over  the  neck  and  other  parts  of  the  body,  or  pallor  may  take  the 
place  of  a  blush  owing  to  vaso-motor  spasm.  Neurasthenic  patients 
are  very  liable  to  suffer  from  cold  hands  and  feet,  which  are  sometimes 
bathed  in  a  clammy  sweat  and  at  other  times  abnormally  dry ;  they 
also  complain  of  coldness  of  the  knees  and  other  joints,  and  chills 
passing  along  the  spine,  all  of  them  being  symptoms  which  may  be 
attributed  to  disorder  of  the  vaso-motor  system. 

The  organic  functions  are  profoundly  affected  in  cerebral  neurasthenia. 
The  heart  is  irritable,  its  action  is  often  tumultuous,  and  the  patient  is 
painfully  sensible  of  its  beatings.  The  pulse  is  compressible,  irregular, 
and  increased  in  frequency,  and  may  on  slight  exertion  beat  one  hundred 
times  or  more  in  the  minute.  Some  of  the  most  distressing  symptoms 
are  caused  by  nervous  dyspepsia  (apepsia  nervosa).  The  patient  may 
take  a  fair  quantitity  of  food  at  a  meal  although  he  is  never  really 
hungry  and  scarcely  ever  feels  as  if  the  stomach  were  quite  empty.  It 
seems  as  if  a  portion  of  the  food  were  always  retained  owing  to  the 
inability  of  the  stomach  to  empty  itself  from  simple  inertia,  and  a  certain 
degree  of  dilatation  of  the  organ  may  be  discovered  on  physical  ex- 
amination. The  introduction  of  fresh  food  into  the  stomach  often  brings 
a  sense  of  relief  and  comfort,  but  it  is  only  of  short  duration,  and  soon 
after  a  meal  the  patient  experiences  a  painful  feeling  of  distention  in 
the  epigastrium,  a  sensation  of  fulness  in  the  head,  confusion  of  thought, 
an  indisposition  to  undertake  any  work,  and  a  sense  of  profound  and 
indescribable  misery.  The  bowels  are  constipated,  or  attacks  of  diarrhoea 
alternate  with  constipation,  and  the  patient  is  much  distressed  with 
flatulent  distention  of  the  abdomen  Avhich  often  becomes  blown  up 
suddenly  in  the  most  unaccountable  manner.  The  urine  is  sometimes 
abundant  and  of  low  specific  gravity,  at  other  times  it  is  unusually  acid 
and  contains  an  excess  of  urates,  while  oxalic  acid  crystals  are  often 
found  in  it. 

The  psycJiical  disorders  are  numerous  and  variable.  One  of  the 
most  constant  is  sleeplessness.  Some  patients  sleep  soon  after  going  to 
bed,  but  awake  with  a  start  in  the  early  morning,  and  are  unable  to  fall 
asleep  again.  This  start  is  often  very  painful,  the  patient  sometimes 
experiencing  a  feeling  as  if  he  had  received  a  blow  with  a  heavy  mallet 


582      FUNCTIONAL    DISEASES    OF    THE    NERVOUS    SYSTEM. 

on  the  top  of  the  head.  In  other  cases  the  subject  lies  awake  for  hours 
after  going  to  bed  and  sleeps  best  in  the  morning.  In  almost  all  cases 
the  sleep  is  disturbed  by  dreams  which  are  always  of  a  disagreeable 
character,  and  in  the  morning  the  sufferer  rises  unrefreshed  and  with  a 
dull  aching  head. 

The  patient  is  liable  to  suffer  from  morbid  fears,  which  may  assume 
various  forms  in  difterent  cases.  The  chronic  hypochondriacal  patient, 
who  goes  from  physician  to  physician  and  from  hospital  to  hospital  wich 
the  fixed  idea  that  he  is  the  subject  of  every  imaginable  disease,  is  well 
known,  but  many  other  varieties  of  morbid  fear  are  met  with  in  neuras- 
thenia. The  following  morbid  fears  have  received  separate  names : 
Astrophobia,  fear  of  lightning ;  topophobia,  fear  of  places,  including 
agoraphobia,  fear  of  open,  and  claustrophobia,  fear  of  narrow  places ; 
anthrophobia,  fear  of  men  and  of  society  generally,  mcin^xng  gynephobia, 
a  special  fear  of  women  ;  monophobia,  fear  of  being  alone  ;  pathophobia, 
fear  of  disease  ;  photophobia,  fear  of  light ;  and  mysophobia,  fear  of 
contamination.  In  addition  to  these  many  other  unreasoning  fears 
might  be  mentioned,  such  as  a  dread  of  poverty,  which,  even  in  cases 
in  which  the  fear  is  not  altogether  groundless,  becomes  morbidly  ex- 
aggerated. Another  fear  Avhicli  haunts  the  neurasthenic  patient  is  an 
intense  dread  of  not  fjilling  asleep  on  going  to  bed,  a  dread  which  in 
many  cases  becomes  the  cause  of  the  sleejdessness  which  is  so  much 
feared.  In  some  cases  this  fear  is  so  overpowering  that  the  patient  sits 
in  an  armchair  the  whole  night  rather  than  risk  jroino;  to  bed,  while  at 
other  times  he  will  not  go  to  bed  without  having  a  glass  of  whiskey  or 
some  narcotic.  Such  patients  are,  indeed,  liable  to  develop  a  morbid 
craving  for  stimulants  or  narcotics.  The  power  of  self-control  is 
diminished,  and  if  once  a  neurasthenic  patient  give  way  to  an  illegitimate 
indulgence  or  to  excess  in  a  legitimate  one  the  vice  is  apt  to  acquire  an 
overpowering  mastery  over  him.  In  neurasthenia,  therefore,  the  patient 
is  apt  to  give  way  to  alcoholic  and  sexual  excesses,  and  many  are  prob- 
ably tempted  to  overstep  the  line  which  divides  vice  from  crime. 
<  The  intellectual  condition  of  those  suffering  from  neurasthenia  is  very 
interesting.  The  first  indication  of  commencing  nervous  exhaustion 
may  be  an  unwonted  difficulty  in  recalling  the  names  of  individuals. 
In  a  further  stage  of  this  amnesia  the  patient  forgets  the  names  of 
familiar  objects  and  he  has  frequently  to  indicate  his  meaning  by  a 
jDaraphrase;  for  example,  he  may  have  to  call  a  "chair,"  "the  thing 
yon  are  sitting  upon."  I  have  known  a  person  suffering  from  neuras- 
thenia who  had  the  greatest  possible  difficulty  in  completing  a  simple 
sentence,  owing  to  his  forgetfulness  of  the  names  of  objects,  and  to 
maintain  a  conversation  for  a  brief  period  required  an  intense  effort 


NEURASTHENIA.  583 

which  was  followed  by  profound  exhaustion.  In  other  cases  the  patient 
is  able  to  converse  freely,  but  is  unable  to  write  a  letter  without  dan- 
ger of  misspelling  simple  words  and  committing  mistakes  in  grammar 
and  diction.  But  a  man  who  is  apt  to  forget  the  name  of  his  most  in- 
timate friend,  who  is  exhausted  by  having  to  carry  on  a  brief  con- 
versation, who  is  unable  to  write  a  simple  business  letter,  and  who  can- 
not concentrate  his  attention  for  more  than  a  few  minutes  at  a  time 
upon  any  ordinary  subject,  may  be  quite  capable  of  grasping  as  Avell  as 
ever  the  profoundest  speculations  of  philosophy.  Educated  men,  indeed, 
have  a  tendency,  when  their  nervous  systems  become  exhausted,  to  brood 
over  such  questions  as  the  relation  between  mind  and  matter,  the  doc- 
trines of  free  will  and  necessity,  the  existence  of  evil,  the  nature  of  the 
first  cause,  and  the  other  great  insoluble  problems  of  the  universe.  And 
it  may  be  taken  as  one  of  the  first  indications  of  recovery  when  the 
patient  is  able  to  set  his  mind  free  from  these  all-absorbing  questions 
and  becomes  again  interested  in  the  practical  details  of  life. 

In  disposition  the  patient  is  shy,  and  to  strangers  he  is  reserved,  but 
he  is  apt  to  exhaust  the  patience  of  his  friends  by  interminable  com- 
plaints of  his  morbid  feelings  and  suiferings.  The  degree  of  shyness 
which  the  patient  manifests  may  vary  from  simple  coyness  to  a  condition 
in  which  he  is  utterly  unable  to  enter  any  kind  of  society,  and  avoids 
converse  with  anyone  except  a  few  intimate  friends.  We  have  already 
seen  that  the  patient  blushes  or  becomes  pale  on  the  slightest  provocation, 
and  when  conversing  with  a  stranger  he  averts  his  eyes,  or  he  may  be 
unduly  watchful  and  have  a  slight  staring  expression  as  if  he  were  try- 
ing to  read  what  is  being  thought  of  him.  In  manner  he  is  fidgetty 
and  frequently  changes  his  position ;  his  hands  are  in  constant  move- 
ment and  he  either  nervously  pulls  his  beard  or  seizes  and  displaces 
small  objects  which  may  be  near  him  ;  his  expression  is  changeable  but 
always  self-conscious ;  his  voice  is  feeble,  in  aggravated  cases  the  patient 
experiences  difficulty  in  articulating  polysyllabic  words ;  and  even  the 
manner  in  which  he  shakes  hands  is  lacking  in  energy. 

The  symptoms  of  neurasthenia  usually  make  their  appearance  between 
the  sixteenth  and  fiftieth  year  of  age,  and  the  attack  generally  super- 
venes when  the  mind  is  subjected  to  some  unusual  strain  or  worry.  The 
symptoms  are  exceedingly  variable  and  it  is  impossible  to  draw  the  line 
which  separates  neurasthenia  from  hysteria  on  the  one  hand  and  melan- 
cholia on  the  other.  The  duration  of  the  affection  depends  greatly 
upon  the  circumstances  and  surroundings  of  the  patient.  If  the  symp- 
toms have  been  induced  by  overwork,  and  it  be  possible  for  the  patient 
to  suspend  work  and  take  a  long  holiday,  the  improvement  usually 
appears  early  and  proceeds  to  complete  recovery.     But  even  in  such 


584:      FUNCTIONAL    DISEASES    OF    THE    NERVOUS    SYSTEM. 

circumstances  it  is  not  always  easy  to  shield  the  patient  from  family 
troubles  and  anxieties,  and  it  may  be  still  less  possible  to  protect  him 
from  the  consequences  of  previous  imprudence  and  immorality.  But, 
although  the  aiFection  is  very  variable  in  its  duration,  it  nearly  always 
terminates  in  recovery,  and  neurasthenic  patients  are  often  long-lived, 
being  less  liable  than  others  to  the  degenerative  changes  of  the  blood- 
vessels and  other  tissues  which  indicate  age  and  shorten  life. 


III.  HEADACHE  (CEPHALALGIA). 

Headache  is  so  important  a  sign  of  nervous  disease  and  arises  from 
so  many  different  causes  that  it  demands  separate  consideration.  The 
following  varieties  may  be  distinguished  : 

(1)  Ancemic  headache  usually  affects  the  temples  and  brow,  or  ex- 
tends along  the  sagittal  suture.  It  is  aggravated  by  long  maintenance 
of  the  erect  posture,  and  by  all  causes  which  exhaust  the  nervous 
system,  such  as  anxiety,  night  watching,  and  sexual  excess ;  while  it  is 
relieved  by  rest  in  the  recumbent  posture. 

(2)  Hypercemic  or  conyemtive  headache  usually  affects  the  Avhole  head  ; 
the  eyes  are  suffused  ;  the  carotids  pulsate  strongly  ;  and  the  headache 
is  accompanied  b}^  throbbing,  agitation,  hypemcsthesia  with  illusions  of 
the  special  senses,  and  sometimes  by  redness  and  heat  of  the  brow  and 
vertex. 

(3)  ITysterical  headache  occurs  in  females  and  is  generally  accom- 
panied by  other  symptoms  of  hysteria.  The  pain  is  sometimes  diffused 
and  deep-seated,  but  it  is  more  frequently  localized  in  one  spot,  and  feels 
as  if  a  nail  were  being  driven  through  the  skull ;  hence  it  is  called 
clavus.  Hysterical  headache  is  increased  in  severit}^  during  the  men- 
strual period  and  by  mental  worry,  whilst  it  is  removed  by  amusement 
and  anything  which  engages  the  attention. 

(4)  Toxic  headaches  are  caused  by  poisons  in  the  circulation.  One 
of  the  best  known  examples  of  this  form  of  headache  is  that  which 
follows  alcoholic  intoxication.  In  the  morning  after  a  carouse  a  severe 
headache  is  experienced,  which  is  chiefly  localized  in  the  deeper  parts  of 
the  eyes  and  at  the  base  of  the  brain,  and  is  accompanied  by  a  feeling  of 
pressure  and  weight.  Severe  headaches  also  follow  the  use  of  narcotics 
and  anaesthetics,  and  the  inhalation  of  various  gases,  such  as  carbonic 
oxide,  sulphuretted  hydrogen,  the  impure  atmosphere  of  crowded  rooms, 
and  sewer  gas.  Obstinate  cephalalgia  is  likeAvise  one  of  the  most 
common  symptoms  of  uraemia,  and  in  many  cases  of  granular  con- 


HEADACHE.  585 

tracted  kidney,  headache  is  the  chief  symptom  complained  of  when  the 
patient  seeks  medical  advice  for  the  first  time. 

(5)  Pyrexia!  headache  is  probably  a  variety  of  the  congestive  or 
hyperaemic  headache,  but  it  is  accompanied  by  elevation  of  temperature 
and  the  other  symptoms  which  indicate  the  onset  of  an  acute  disease 
such  as  the  specific  fevers  and  acute  inflammatory  diseases  like  pneu- 
monia. The  headache  is  generally  moderate  in  intensity,  dull  and 
deep-seated,  and  is  accompanied  by  a  feeling  of  lightness  in  the  head, 
and  not  infrequently  by  delirium.  This  form  of  headache  ceases,  ac- 
cording to  Jenner,  when  delirium  begins. 

(6)  Neurasthenic  headache  occurs  when  the  nervous  system  is  ex- 
hausted by  mental  anxiety  and  worry,  night  Avatching  or  other  depress- 
ing circumstances.  The  pain  varies  considerably  in  its  character,  but 
it  is  generally  deep-seated,  heavy,  dull,  and  oppressive.  It  is  often 
attended  by  a  feeling  of  pressure  and  tension  above  the  occiput,  and 
often  by  great  sensitiveness  to  touch  in  that  region. 

(7)  Rheumatic  headache  consists  of  a  violent  and  tearing  pain  local- 
ized in  the  muscles  of  the  head,  or  in  the  fascia  of  the  occipito-frontalis 
muscle.  It  is  often  attended  with  marked  tenderness  of  the  scalp,  and 
is  usually  brought  on  by  exposure  to  cold. 

(8)  Gouty  headache  takes  the  form  of  a  dull,  heavy  pain  in  the 
forehead,  and  is  generally  attended  by  great  depression  of  spirits,  gid- 
diness, pain  and  fulness  in  the  right  hypochondrium,  flatulence,  and  a 
high-colored  urine  loaded  with  lithates.  Intense  neuralgiform  head- 
aches, which  are  often  termed  gouty,  are  probably  in  most  cases  an 
expression  of  commencing  granular  changes  in  the  kidneys. 

(9)  Sympathetic  headache  may  supervene  on  disease  of  almost  all 
the  peripheral  organs,  although  it  is  commonly  associated  with  diseases  of 
the  digestive  and  sexual  organs.  The  most  common  form  of  this  variety 
is  the  brow-ache  of  gastric  catarrh,  but  headache  may  accompany  irrita- 
tion of  the  intestinal  canal  or  of  the  uterus  and  ovaries.  This  is  probably 
the  place  in  which  to  mention  the  headache  caused  by  excessive  strain- 
ing of  the  eyes.  This  form  of  headache  is  often  accompanied  by 
vertigo,  insomina,  and  sickness,  and  occasionally  by  vomiting.  Head- 
ache may  be  caused  by  excessive  use  of  the  normal  eye,  but  it  is  much 
more  liable  to  be  induced  when  the  eye  is  deficient  as  an  optical  instru- 
ment, and  is  especially  liable  to  occur  in  disorders  of  accommodation. 
In  cases  of  headache  of  obscure  origin,  and  more  especially  when  it  is 
found  to  supervene  or  to  become  intensified  when  the  patient  begins  to 
read  or  write,  the  state  of  vision  should  be  carefully  investigated  by  an 
ophthalmologist. 

(10)  Syphilitic  headache  is  characterized  by  a  deep-seated  and  in- 


586      FUNCTIOXAL    DISEASES    OF    THE    NERVOUS    SYSTEM. 

tense  pain,  Avhich  is  either  attended  by  a  feeling  of  weight  on  the 
vertex  or  a  sense  of  constriction  as  if  the  head  -were  held  fast  in  a  vice. 
The  patient  compares  it  to  that  which  might  be  caused  by  successive 
blows  on  the  head  with  a  heavy  mallet.  The  pain  is  at  times  distinctly 
circumscribed,  at  other  times  it  is  diffused,  and  may  then  occupy  either 
the  frontal,  temporal,  or  occipital  regions.  In  some  cases  it  is  diffused 
and  invades  the  whole  head.  The  headache  never  completely  intermits, 
but  it  is  liable  to  paroxysmal  exacerbations  of  great  severity,  which 
are  particularly  intense  during  the  night.  There  is,  indeed,  no  other 
form  of  headache  in  which  a  nocturnal  exacerbation  is  so  characteristic 
as  the  syphilitic  variety,  and  it  is  alwaj's  accompanied  by  a  degree  of 
sleeplessness  which  is  often  out  of  proportion  even  to  the  intensity  of 
the  headache. 

(11)  Organic  headache  occurs  as  one  of  the  symptoms  of  structural 
disease  within  the  cranium,  and  is  especially  characteristic  of  intra- 
cranial growths.  The  pain  is  persistent  and  continuous,  but  liable  to 
paroxysmal  exacerbations  of  great  severity.  It  may  be  frontal  or 
occipital,  and  it  is  generally  deeply  seated  in  one  spot,  although  it  may 
extend  over  the  whole  head.  Tenderness  of  the  scalp  often  attends 
the  headache,  and  pain  may  be  elicited  on  percussing  the  skull  over  the 
seat  of  the  tumor.  An  ophthalmoscopic  examination  often  reveals  the 
presence  of  optic  neuritis. 


(12)  Hemicrania. 

Etiology. — The  predisposing  causes  of  hemicrania  are  inheritance, 
generally  from  mother  to  daughter;  a  neuropathic  disposition;  the 
female  sex,  and  the  ages  of  fifteen  to  thirty  years,  while  the  exciting 
causes  are  digestive  disorders,  constipation,  exhaustion  from  want  of 
food,  fatigue,  sleeplessness,  and  excessive  mental  exertion. 

Symptoms. — Hemicrania  consists  of  paroxysms  of  headache  which 
are  separated  by  free  intervals  of  shorter  or  longer  duration.  The 
attack  is  frequently  preceded  by  premonitory  symptoms,  the  patient 
has  a  sense  of  pressure  in  the  head,  and  feels  chilly,  nauseated,  de- 
pressed, Aveary,  and  indisposed  to  work.  Other  interesting  symptoms 
often  precede  the  attack.  The  most  usual  of  these  are  transitory  im- 
pairment of  cutaneous  sensibility,  which  is  accompanied  by  tingling, 
numbness,  and  formication.  At  other  times  there  may  be,  separately 
or  in  various  combinations,  deafness,  tinnitus  aurium,  a  bitter  taste, 
loss  of  taste,  embarrassment  of  speech,  momentary  incoherence,  drowsi- 


HEADACHE.  587 

ness,  transitory  paresis  of  one  of  the  limbs,  vertigo,  indistinct  vision, 
muscre  volitantes,  scintillating  scotoma,  or  hemiopia. 

The  characteristic  pain  comes  on  by  degrees  in  the  course  of  the  day, 
but  almost  never  with  the  lightning  rapidity  of  the  pain  of  neuralgia.  The 
patient  often  feels  great  drowsiness  and  weariness  in  the  evening,  and 
awakens  with  headache  in  the  morning.  It  often  begins  with  a  dull 
pain  over  the  forehead,  and  as  it  increases  in  severity  it  passes  down  to 
one  eye  and  remains  fixed  over  the  temple.  Occasionally  it  is  localized 
at  the  top  or  back  of  the  head.  The  left  is  more  frequently  attacked 
than  the  right  side,  but  occasionally  successive  attacks  occur  on  alter- 
nate sides,  these  cases  being  named  hemicrama  alternans  by  Eulenburg. 
Patients  describe  the  pain  as  being  dull,  burning,  or  bursting,  and  it  is 
frequently  associated  with  an  intense  feeling  of  sickness.  Every  beat 
of  the  heart  is  felt  as  a  throb  of  pain,  and  the  slightest  movement,  even 
raising  the  head  from  the  pillow,  or  the  exertion  of  talking,  augments 
the  throbbing  pain  to  an  almost  unendurable  pitch  by  exciting  the  cir- 
culation. The  patient  suffers  from  continuous  nausea,  the  appetite  is 
lost,  there  may  be  more  or  less  jaundice,  and  the  attack  often  terminates 
by  free  vomiting,  first  of  the  usual  contents  of  the  stomach  and  after- 
wards of  bile.  The  skin  over  the  forehead,  temples,  and  parietal  region 
is  often  sensitive  to  a  light  touch  during  an  attack  of  migraine,  but 
deep  diffused  pressure  affords  relief  Berger  has  shown  that  the  sense 
of  touch  may  become  morbidly  acute  (ht/perpselaphesia),  the  circle  of 
perception  being  sometimes  only  one  line  in  diameter  on  the  affected, 
and  four  lines  on  the  sound  side  of  the  forehead.  He  also  found  that 
variations  of  temperature  of  0.4°  C.  were  perceived  on  the  affected,  and 
only  of  0.8°  C.  on  the  sound  side.  The  electro-cutaneous  sensibility  was 
likewise  increased  on  the  affected  side.  Deep  pressure  over  the  superior 
or  middle  cervical  ganglion  of  the  sympathetic,  and  over  the  spinous  pro- 
cess of  the  cilio-spinal  region  of  the  cord  is  painful,  and  a  small  spot  is 
sometimes  found  over  the  parietal  protuberance  which  is  painful  on  pres- 
sure, but  the  painful  points  of  genuine  neuralgia  are  never  present. 

The  vaso-motor  phenomena  of  migraine  are  exceedingly  important, 
and  the  disease  has  been  divided  into  (1)  hemicrania  spastica  or  sym- 
pathico-tonica,  (2)  hemicrania  angioparalytica  or  neuroparaJytica,  and 
(3)  hemicrania  mixta,  according  as  the  phenomena  of  vascular  con- 
traction, dilatation,  or  first  contraction  and  then  dilatation,  are  present 
respectively. 

1.  Hemicrania  Spastica  or  Sympathico-tonica. — On  the  affected 
side,  at  the  height  of  the  attack,  the  eye  is  prominent ;  the  pupil  is 
dilated ;  the  temporal  artery  feels  like  a  hard  cord ;  the  side  of  the  face 
and  the  ear  are  pale ;  and  the  temperature  in  the  external  meatus  is  lower 


588      FUNCTIONAL    DISEASES    OF    THE    NERVOUS    SYSTEM. 

by  0.4°  C.  or  0.6°  C.  than  that  of  the  meatus  of  the  opposite  side. 
The  pain  is  aggravated  by  every  circumstance  which  excites  the  circu- 
lation and  increases  the  arterial  tension,  and  compression  of  the  carotid 
on  the  aifected  side  augments,  and  of  that  on  the  unaffected  side  dimin- 
ishes the  pain.  The  salivary  secretion  is  much  increased  in  quantity  and 
becomes  very  viscid.  Towards  the  end  of  the  attack  the  affected  side 
of  the  face  and  ear  become  red  and  hot,  the  conjunctiva  is  injected, 
there  is  a  copious  flow  of  tears,  the  pupil  becomes  contracted,  a  diffused 
feeling  of  Avarmth  spreads  over  the  body,  and  the  paroxysm  terminates 
by  palpitations,  vomiting,  a  free  discharge  of  limpid  urine,  and  some- 
times a  watery  evacuation  from  the  bowels. 

2.  Hemicrania  Angioparalytica  or  Neuroparalytica. — On  the  affected 
side,  at  the  height  of  the  attack,  the  eye  is  retracted ;  the  palpebral  fissure 
is  narrowed;  the  pupil  is  contracted;  the  conjunctiva  is  injected;  there 
is  an  increased  flow  of  tears ;  the  side  of  the  face  and  ear  are  red,  hot, 
and  turgid;  the  temporal  artery  is  large,  tortuous,  and  beats  with 
unusual  force;  and  the  temperature  in  the  external  meatus  is  higher 
by  from  0.2°  C.  to  0.4°  C.  than  on  the  opposite  side;  and  compres- 
sion of  the  carotid  on  the  affected  side  and  of  that  on  the  opposite 
side  aggravates  the  pain.  The  radial  artery  is  sometimes  small  and 
contracted,  and  the  pulse  is  slow,  beating  only  from  forty-eight  to  fifty- 
six  times  a  minute.  Towards  the  end  of  the  attack  the  face  becomes 
paler  and  the  other  phenomena  pass  off.  Vomiting  is  not  so  urgent  a 
symptom  in  the  paralytic  as  in  the  spastic  variety,  and  the  course  of 
the  former  is,  on  the  wliole,  milder  than  that  of  the  latter, 

3.  Hemicrania  Mixta. — In  this  form  the  phenomena  of  the  spastic 
variety  are  present  at  first,  but  these  are  soon  followed  by  those  of  the 
paralytic  variety. 

An  attack  of  hemicrania  usually  lasts  from  a  few  liours  to  half  a 
day,  but  may,  at  times,  continue  a  whole  day  or  even  several  days. 
If  the  pain  be  present  on  waking  it  often  wears  off  gradually  towards 
evening,  and  the  patent  falls  into  a  sleep  from  which  he  usually  awakes 
free  from  pain.  But  if  it  should  come  on  during  the  day,  it  gradually 
increases  in  severity,  and  the  patient  is  unable  to  sleep.  The  headache 
is  generally  most  tolerable  when  the  patient  is  laid  down  in  a  darkened 
room,  but  at  other  times  it  is  aggravated  by  the  recumbent  position, 
and  the  patient  can  best  endure  his  suflerings  in  the  sitting  or  upright 
posture.  The  paroxysms  often  recur  with  great  regularity  at  intervals 
of  three  or  four  weeks,  and  females  are  frequently  attacked  during  the 
catamenial  period,  although  this  rule  is  not  without  numerous  excep- 
tions. Those  who  are  liable  to  migraine  often  enjoy  excellent  health 
during  the  intervals  between  the  attacks.     Migraine  headaches  fre- 


HEADACHE.  5§9 

quently  cease  to  recur  after  the  climacteric  jDeriod  in  women,  and  after 
the  fiftieth  year  of  age  in  men,  and  in  persons  Avho  do  not  inherit  a 
strong  tendency  to  the  disease  they  may  cease  at  an  early  ao-e,  either 
spontaneously  or  under  the  influence  of  remedies. 

3Iorhid  Physiology. — In  sjnnal  irritation  there  is  an  excessive  irrita- 
bility of  the  spinal  cord,  but  the  brain  also  must  participate  in  this  dis- 
order, inasmuch  as  the  spinal  symptoms  are  usually  associated  with  an 
emotional  condition,  such  as  is  met  with  in  hysteria.  It  must  be  remem- 
bered that  the  inci'eased  irritability  of  the  nervous  tissues  in  spinal 
irritation  is  a  paralytic  irritability  and  therefore  the  afiection  is  allied 
to  exhaustion  of  the  nervous  system  or  to  neurasthenia. 

Neurasthenia  is,  as  its  name  implies,  caused  by  exhaustion  of  the 
nervous  system,  those  portions  of  it  which  are  the  last  to  be  developed 
being  more  profoundly  afiected  than  the  earlier  evolved  parts.  Ex- 
haustion of  the  latest  evolved  tissues  implies  diminution  or  temporary 
abolition  of  the  latest  evolved  functions,  and  consequently  the  control 
of  the  conscience  is  diminished,  and  the  animal  instincts  and  propensi- 
ties become  more  urgent  and  active.  But  although  the  stock  of  energy 
of  the  nervous  system  is  diminished ^the  irritability  is  increased,  just  as 
occurs  in  the  nervous  tissues  of  animals  after  prolonged  starvation. 
The  consequence  is  that  stimuli  which  produce  little  or  no  effect  in 
health  have  now  widespread  results.  This  excessive  irritability  of  the 
nervous  tissues  explains  the  great  mental  excitability  of  neurasthenic 
patients,  as  well  as  their  sensitiveness  to  changes  of  weather  and  other 
external  stimuli. 

Hemicrania  is  the  only  form  of  headache,  the  morbid  physiology  of 
which  we  shall  discuss  in  this  place.  The  chief  symptoms  which  re- 
quire explanation  are  (1)  the  vaso-motor  and  oculo-pupillary  symptoms, 
(2)  the  disorders  of  the  general  circulation,  and  (3)  the  pain. 

(i)  The  vaso-motor  and  oculo-piqnllary  disorders  which  are  observed 
in  hemicrania  spastica  are  explained  by  supposing  that  the  cilio-spinal 
region  of  the  spinal  cord  and  the  cervical  sympathetic  are  in  a  state  of 
irritation,  those  of  hemicrania  paralytica  by  supposing  that  the  same 
nervous  mechanism  is  paralyzed,  and  those  of  mixed  hemicrania  by 
supposing  that  this  mechanism  is  first  irritated  and  then  paralyzed. 

(2)  The  retardation  of  the  pulse  which  is  often  observed  is  supposed 
by  Landois  to  be  due  to  direct  irritation  of  the  vaso-motor  centre  in 
the  medulla.  Other  symptoms  which  show  that  this  centre  is  in  a  state 
of  irritation  are  coldness  of  the  hands,  chilliness,  suppression  of  per- 
spiration, contracted  state  of  the  radial  artery,  and  increased  arterial 
tension.  Towards  the  end  of  the  attack  symptoms  of  vascular  dilata- 
tion, such  as  increased  secretion  of  saliva  and  urine,  and  watery  stools 


590      FUNCTIONAL    DISEASES    OF    THE    NERVOUS    SYSTEM. 

indicate  that  the  irritation  of  the  vaso-motor  centre  has  been  followed 
by  exhaustion  and  temporary  paralysis. 

(3)  The  pain  in  migraine  has  been  variously  explained.  Romberg 
thought  it  due  to  a  hyper?esthesia  of  the  brain,  and  he  called  it  "  neu- 
ralgia cerebralis  "  in  order  to  distinguish  it  from  peripheral  neuralgia. 
Others  suppose  that  the  pain  is  caused  by  a  neuralgia  of  the  intra- 
cranial and  meningeal  branches  of  the  trigeminus  and  the  other  nerves 
which  accompany  the  bloodvessels,  and  not  of  the  cerebrum  itself  as 
Romberg  supposed.  But  when  once  the  vaso-motor  and  oculo-pupillary 
symptoms  of  hemicrania  attracted  attention  the  supposition  that  the 
pain  was  secondary  to  vascular  disturbances  in  the  brain  lay  near  at 
hand.  Du  Bois-Reymond  suggested  that  the  pain  was  caused  by  a  tonic 
spasm  of  the  muscular  coat  of  the  vessels  and  was  thus  similar  to  the 
pain  felt  in  cramp  of  the  muscles,  or  to  that  felt  in  the  uterus  during 
labor.  Others  have  suggested  that  the  pain  is  caused  by  the  anaemia 
which  results  from  spasm  or  the  hypememia  which  results  from  dilata- 
tion of  the  vessels  of  the  brain;  this  view  being  supported  by  the  well- 
known  fact  that  anaemia  or  hyperaemia  of  the  peripheral  nerves  is  one 
of  the  most  frequent  causes  of  various  neuralgias.  But  some  pathol- 
ogists believe  that  hemicrania  is  allied  to  genuine  epilepsy.  The  facts 
in  fiivor  of  this  opinion  are  the  paroxysmal  character  of  the  disease,  its 
occurrence  in  members  of  neuropathic  families,  and  the  attack  being 
often  preceded  by  symptoms,  like  scintillating  scotoma,  resembling  an 
epileptic  aura  and  occasionally  accompanied  by  embarrassment  of  speech 
or  a  slight  degree  of  aphasia.  Observing  the  resemblances  between 
certain  forms  of  headache  and  epilepsy  Dr.  Sieveking  proposed  to  name 
the  periodical  headaches  of  nervous  peoi)le  cephalalgia  epileptica,  while 
Dr.  Liveing  for  the  same  reason  came  to  the  conclusion  that  hemicrania 
was  caused  by  "  nerve  storms."  But  Dr.  Hughlings-Jackson  has  given 
a  more  scientific  expression  to  this  theory  by  attributing  the  headache 
of  migraine,  especially  the  form  which  is  associated  with  ocular  phe- 
nomena, to  a  discharging  lesion  from  the  cortex  of  the  posterior  lobes 
or  the  sensory  area  of  the  brain,  or  in  that  part  of  the  sensory  area 
which  is  the  anatomical  correlative  of  the  sensation  of  pain  in  the  head. 
But  during  the  attack  the  nervous  discharge  does  not  remain  limited  to 
the  sensory  area,  since  some  is  directed  outwards  to  the  medulla  oblongata 
and  cilio-spinal  region  of  the  spinal  cord,  causing  irritation  or  inhibition 
of  some  of  these  centres,  and  giving  rise  to  the  vaso-motor  and  oculo- 
pupillary  phenomena  of  the  disease. 

Ti'eatment. — The  treatment  of  spinal  irritation  must  first  be  directed 
to  remove  the  cause,  while  an  endeavor  is  made  to  improve  the  general 
nutrition  by  a  full  diet  including  the  moderate  use  of  wine,  and  much 


HEADACHE.  591 

exposure  to  the  open  air  and  to  sunlight.  The  patient  should  rest  fre- 
quently in  the  recumbent  posture,  and  all  causes  of  fatigue  should  he 
avoided.  Change  of  air  to  a  dry  mountainous  district  or  to  the  seaside, 
or  a  moderate  hydropathic  treatment  may  be  found  useful. 

The  internal  remedies  which  are  found  most  generally  useful  are 
quinine,  iron,  zinc,  and  strychnine.  The  galvanic  current  should  be 
passed  through  the  vertebral  column,  and  the  painful  portions  should  be 
included  between  the  poles.  Each  sitting  should  be  short  and  the 
strength  of  the  current  moderate.  The  negative  pole  placed  directly 
over  the  painful  vertebra  appears  to  be  a  good  method  of  applyin<T 
galvanism,  and  general  faradization  or  central  galvanization  is  said  to 
be  useful.  Counter-irritation  applied  directly  over  the  painful  portion 
of  the  spine  is  a  most  effectual  method  of  treatment  and  Corrio-an's 
button  gives  very  favorable  results. 

Neurasthenia  must  be  treated  on  the  same  general  principles  as  spinal 
irritation.  The  means  to  be  adopted  are  complete  mental  rest,  generous 
diet,  and  much  exposure  to  fresh  air  and  sunlight,  but  with  only  a 
moderate  amount  of  active  exercise.  It  is  almost  incredible  what  a 
small  amount  of  exercise  suffices  to  induce  great  fatigue  followed  by 
profound  mental  depression  in  such  patients,  even  when  the  subject 
of  the  disease  appears  to  be  possessed  of  great  muscular  strength.  In 
aggravated  cases  the  treatment  introduced  by  S.  Weir  Mitchell  of  rest, 
seclusion,  over-feeding,  electricity,  and  massage,  should  be  adopted. 

The  treatment  of  headache  may  be  directed  against  the  cause,  or 
against  the  symptom  of  pain.  In  order  to  fulfil  the  first  indication  the 
remedies  for  anaemia,  hyperasmia,  hysteria,  syphilis,  nervous  exhaustion, 
Bright's  disease,  or  for  allaying  local  irritations  must  be  employed  ac- 
cording to  the  nature  of  case. 

It  is  scarcely  possible  to  adopt  a  casual  treatment  against  migraine, 
inasmuch  as  so  little  is  known  of  the  circumstances  which  concur  to 
induce  an  attack.  An  emetic  may  sometimes  arrest  an  impending 
attack,  but  it  appears  to  act  less  by  removing  indigestible  substances 
than  by  the  impression  it  produces  upon  the  nervous  system. 

The  direct  treatment  of  migraine  may  be  divided  into  that  which  is 
appropriate  during  the  intervals  and  for  removing  or  palliating  the 
paroxysm.  In  the  intervals  between  the  attacks  the  preparations  of 
iron,  especially  the  carbonate,  have  been  found  useful  in  feeble  and 
amemic  subjects.  Arsenic  is  another  very  useful  drug  during  tlie 
intervals,  and  other  periodic  remedies,  such  as  quinine,  quinoidin,  and 
salicin,  have  been  tried,  but  they  appear  to  act  better  in  arresting  an 
impending  attack  than  during  the  interval.  Strychnine,  nitrate  of  silver, 
sulphate  of  nickel,  bromide  of  potassium,  chloride  of  ammonium,  oil  of 


592      FUNCTIONAL    DISEASES    OF    THE    NERVOUS    SYSTEM. 

turpentine,  and  lupulin  have  been  tried  during  the  interval,  but  with 
doubtful  success.  Chalybeate  springs,  mud  and  sea  baths,  hydropathy, 
and  residence  in  lofty  mountainous  regions,  have  all  been  found  bene- 
ficial, but  they  appear  to  influence  the  disease  favorably  by  improving 
the  general  health.  Dr.  Ringer  believes  that  cannabis  indica  in  doses 
of  from  one-quarter  to  one-half  a  grain,  or  ten  minims  of  the  tincture 
three  times  a  day,  is  one  of  the  best  remedies  we  possess  for  preventing 
the  attack.  In  the  treatment  of  the  attack  every  source  of  external 
irritation  should  be  removed,  the  room  should  be  moderately  darkened, 
and  all  noises  should  be  prevented.  In  spastic  hemicrania  the  patient 
should  lie  flat  on  the  back  with  the  head  a  little  raised,  Ijut  in  the 
paralytic  variety  the  patient  usually  prefers  to  maintain  a  sitting  posture, 
and  to  rest  the  head  against  some  hard  substance.  Firm  compression 
of  the  head  by  a  handkerchief  bound  round  it  is  an  old  remedy  and 
appears  to  give  temporary  relief.  The  application  of  cold  to  the  head 
by  means  of  an  evaporating  lotion  or  ice  bag  is  often  grateful,  while  a 
warm  fomentation  to  the  forehead  and  temple  is  sometimes  more  soothing 
than  the  cold.  Quinine  given  in  doses  of  from  five  to  fifteen  grains 
two  or  three  times  in  succession  often  arrests  an  attack,  and  half  drachm 
doses  of  the  liquid  extract  of  ergot  are  often  useful  in  the  angioparalytic 
variety. 

Coffee  is  another  remedy  which  appears  to  act  by  stimulating  the 
vaso-motor  nerves,  and  may  be  given  in  the  form  of  a  strong  infusion, 
but  its  alkaloid,  caffeine,  is  more  eff'ectual.  The  citrate  of  caffeine  may 
be  ordered  in  doses  of  one  grain  every  four  hours  for  some  time  before 
the  expected  attack.  Guarma  powder  in  half  drachm  doses  every  four 
hours  till  relief  is  obtained  is  sometimes  very  effectual.  The  inhalation 
of  the  nitrite  of  amyl  has  been  found  useful  in  the  spastic  form  of 
hemicrania,  but  it  acts  only  as  a  palliative,  its  effect  being  transitory. 

Croton  chloral  hydrate  is  a  very  useful  remedy  for  arresting  the  attack. 
It  may  be  administered  in  five  grain  doses  every  four  hours  or  in  one 
dose  of  from  fifteen  to  twenty  grains.  The  late  Dr.  Austin  thought 
the  best  means  of  arresting  a  sick  headache  was  to  give  twenty  grains 
of  chloral  and  make  the  patient  plunge  his  feet  into  very  hot  water  and 
mustard  while  breathing  the  steam.  A  full  dose  of  bromide  of  potas- 
sium either  alone  or  in  combination  Avith  chloral  or  Avith  tincture  of 
opium,  or  better  still  nepenthe,  is  also  very  efficacious.  Chloride  of 
ammonium  in  half  drachm  doses  is  another  useful  remedy.  Morphia 
and  other  narcotics  may  be  employed  in  aggravated  cases,  but  they  are 
not  so  useful  in  migraine  as  in  neuralofia. 

The  galvanic  current  when  properly  applied  is  one  of  the  most  power- 
ful remedies  we  possess  for  hemicrania.     Hoist  recommends  that  one 


HEADACHE.  593 

electrode  be  placed  at  the  inner  edge  of  the  sterno-cleido-mastoid  muscle, 
and  the  other  on  the  palm  of  the  hand.  The  pole  on  the  neck  is  made 
l)0sitive  in  hemicrania  spastica,  and  from  ten  to  fifteen  elements  are 
used  for  two  or  three  minutes,  while  the  negative  pole  is  used  at  the 
neck  in  hemicrania  angioparalytica  and  powerful  excitations  are  pro- 
duced by  re})eated  closures  and  openings,  or  by  reversals.  Other  authors 
recommend  that  a  weak  current  should  be  passed  continuously  through 
the  head.  The  induced  current  has  been  recommended  by  Frominhold  ; 
he  applies  one  of  the  poles  high  up  the  back  of  the  neck  in  the  median 
line,  and  the  other  upon  the  forehead  or  over  the  superciliary  arch. 
Fieber  employs  the  "  electric  hand,"  and  the  application  is  certainly 
grateful  to  the  patient,  but  I  have  not  found  that  it  produces  a  marked 
effect  upon  the  duration  of  the  attack. 

In  dealing  Avith  the  various  forms  of  headache,  other  than  hemicrania, 
the  treatment  must  be  directed  against  the  cause  of  the  pain.  In  the 
anaemic  form,  iron  and  sustaining  diet ;  in  the  hypersemic,  saline  pur- 
gatives and  low  diet ;  in  the  febrile,  ice  to  the  head  ;  in  the  hysterical, 
iron  and  moral  management  of  the  patient,  are  the  means  of  treatment 
which  must  be  chiefly  relied  upon.  In  symptomatic  headache  the 
stomach  or  other  organ  which  is  the  source  of  irritation  must  be  sub- 
jected to  treatment ;  in  gouty  headache  with  hepatic  derangement  saline 
purgatives  bring  relief;  and  in  the  neuralgiform  variety  saline  diuretics 
and  agents  which  lower  the  arterial  tension  are  indicated.  In  rheumatic 
headache  salicylate  of  soda  may  be  given,  but  iodide  of  potassium  is,  as 
a  rule,  the  most  effectual  remedy  for  such  cases.  In  syphilitic  headache 
an  energetic  antisyphilitic  treatment  must  be  adopted. 


38 


CHAPTEK    XIY. 

SHOCK,  CONCUSSION,  AND  ALLIED  CONDITIONS. 

I.  SHOCK. 

Etiology. — Shock  is  more  easily  produced  in  persons  inheriting  an 
irritable  and  unstable  nervous  system  than  in  robust  persons,  in  Avomen 
than  in  men,  and  in  young  than  in  old  people.  The  exciting  causes  of 
shock  are  sudden  and  severe  or  extensive  injuries  of  any  part  of  the 
body,  and  strong  emotional  excitement,  especially  the  depressing  pa.ssions. 

Symptoms. — Cases  of  shock  may  be  divided  clinically  into  two,  (1) 
torpid  shock  or  those  in  Avhich  the  symptoms  of  depression  predominate, 
and  (2)  erethismic  shock  or  those  in  which  the  symptoms  of  prostration 
are  associated  with  those  of  excitement. 

(1)  Torpid  SJiocJc. — In  the  torpid  form  of  shock  the  patient  lies 
utterly  prostrate,  the  surface  of  the  body  is  pale,  cold,  and  covered  by 
a  clammy  sweat,  which  collects  in  drops  on  the  forehead  and  eyebrows ; 
the  lips  are  bloodless,  the  nostrils  dilated,  and  the  countenance  of  a 
dull  aspect  and  shrunken  ;  while  the  eyes  have  lost  their  lustre,  are  sunk 
in  their  sockets,  and  partially  concealed  by  the  drooping  lids.  There  is 
complete  muscular  relaxation,  which  may  even  extend  to  the  sphincters. 
If  the  patient  be  conscious  he  may  complain  of  feeling  cold  and  faint, 
and  the  whole  body  may  tremble.  The  pulse  is  frequent,  unequal,  and 
feeble  or  imperceptible  at  the  Avrist,  but  the  fluttering  action  of  the  heart 
may  be  heard  on  auscultation.  The  respiratory  movements  are  irregular 
and  gasping,  or  short  and  feeble,  the  respirations  being  sometimes  so 
feeble  that  they  are  scarcely  visible,  although  a  slight  movement  of  the 
diaphragm  may  generally  be  discovered  by  careful  observation.  The 
temperature  of  the  body  is  depressed.  The  patient  suffers  from  vertigo 
and  dimness  of  vision,  while  in  the  less  severe  cases  there  are  nausea, 
vomiting,  and  hiccough.  The  psychical  symptoms  consist  of  mental 
depression,  restlessness,  confusion  of  thought,  incoherence,  or  drowsiness, 
but  the  patient  generally  gives  rational  replies  to  definite  questions.  At 
other  times  the  patient  appears  singularly  calm  and  rational,  while  the 
various  senses  remain  unaffected,  hearing  being  sometimes  unusually 
acute. 


SHOCK.  595 

(2)  Erethismie  Shock. — This  form  of  shock  is  rare,  the  majority  of 
cases  in  which  symptoms  of  prostration  are  mixed  with  those  of  excite- 
ment being  preceded  by  a  distinct,  though  it  may  be  transient  stance  of 
collapse.  The  skin  is  at  first  hot  and  dry ;  the  pulse  is  quick  and 
bounding,  but  always  compressible ;  the  respirations  are  hurried,  imper- 
fect, and  interrupted  by  sighs ;  the  tongue  is  tremulous ;  the  patient 
complains  of  thirst ;  rigors  are  occasionally  present ;  and  vomiting  is  a 
frequent  and  sometimes  obstinate  symptom.  The  mental  and  bodily 
prostration  of  collapse  is  succeeded  by  tremor  and  twitchings  of  the 
muscles,  and  the  patient  suffers  from  restlessness,  jactitation,  prsecordial 
anxiety,  and  delirium.  At  times  the  patient  merely  presents  a  peculiar 
irritability  of  manner  with  an  increased  disposition  to  talk,  sometimes 
rationally,  occasionally  incoherently.  At  other  times  the  patient  has 
strange  illusions  attended  by  a  peculiar  dread  of  impending  evil. 

In  some  cases,  however,  there  is  fierce  maniacal  raving,  which  is  most 
pronounced  during  the  night,  or  the  delirium  may  assume  all  the  charac- 
teristics of  that  observed  in  delirium  tremens.  The  patient  obtains  no 
sleep,  or  it  is  partial,  interrupted,  and  unrefreshing.  As  the  exhaustion 
increases  the  skin  is  covered  by  a  cold,  clammy,  and  often  profuse 
sweat;  the  face  becomes  pale;  the  expression  haggard;  and  the  pulse 
is  frequent,  irregular,  fluttering,  and  uncontrollable.  Towards  the  end 
subsultus  and  slight  convulsions  supervene  and  the  patient  dies  coma- 
tose. In  the  severest  form  of  shock  the  functions  of  the  nervous 
system  are  suddenly  abolished  and  the  heart  ceases  to  beat;  in  the 
mild  forms  of  the  affection  the  symptoms  are  more  or  less  similar  to 
those  of  an  ordinary  fainting  fit,  while  between  these  two  kinds  in- 
numerable transitional  forms  are  observed.  The  medium  degrees  of 
shock  are  named  collapse.  In  the  intermediate  forms  of  shock  the 
symptoms  of  collapse  give  place  to  those  of  excitement,  this  stage 
being  called  the  period  of  reaction.  The  period  of  reaction  is  charac- 
terized by  improved  pulse  and  respiration,  restoration  of  muscular 
power,  and  increase  of  temperature.  These  symptoms  often  merge 
quickly  into  health,  but  in  some  cases  relapses  occur,  and  convalescence 
is  then  protracted.  In  other  cases  the  torpid  may  be  replaced  by  the 
erethismie  form  of  the  disease.  Recovery  after  shock  is  often  partial 
only,  the  irritability  of  the  nervous  system  remains  permanently  in- 
creased, so  that  slight  exciting  caases  suffice  to  give  rise  again  to  the 
phenomena  of  shock. 


696      SHOCK,  CONCUSSION,    ANT)    ALLIED    CONDITIONS. 

II.  CONCUSSION  OF  THE  SPINAL  COED  (COMMOTIO  SPINALIS). 

Etiology. The  most  usual  causes  of  spinal  concussion  are  falls  upon 

the  feet  or  buttocks,  blows  over  the  back,  and  railway  collisions,  those 
who  sit  with  their  back  in  the  direction  from  which  the  shock  comes 
being  most  liable  to  suffer.  Lightning  passing  through  the  body  causes 
a  general  shock  in  which  the  spinal  cord  participates,  and  violent 
mental  excitement  appears  to  l)e  able  to  produce  the  symptoms  of  spinal 
concussion  occasionally. 

Symptoms. — The  most  usual  symptoms  of  spinal  concussion  are 
feebleness  or,  on  rare  occasions,  paralysis  of  the  extremities;  paraes- 
thesise  of  various  kinds;  pain  in  the  neck,  loins,  or  along  the  spinal 
column;  tenderness  on  pressure  of  some  of  the  spinous  processes; 
some  deforce  of  cutaneous  hypergesthesia  or,  more  often,  anaesthesia, 
weakness  of  the  bladder,  and  considerable  emotional  disturbance. 


Varieties  of  Spinal  Concussion. 

(1)  Severe  Forms  of  Shock  causing  Rapid  Death. — The  patient, 
after  the  injury,  is  found  more  or  less  paralyzed  in  all  his  extremities: 
the  surface  of  the  body  is  distinctly  anaesthetic;  the  pulse  is  small, 
weak,  and  slow ;  the  skin  is  cold  and  pale  or  slightly  cyanotic ;  the  res- 
piration is  disordered  and  sometimes  the  difficulty  of  breathing  may 
amount  to  dyspnoea;  the  mind  is  confused  or  there  may  be  complete 
loss  of  consciousness;  the  stools  and  urine  are  passed  involuntarily; 
and  the  patient  dies  in  a  few  hours  or  days  from  general  prostration 
and  paralysis  of  respiration. 

(2)  Slight  Shock  causing  Severe  Symptoms  at  first.,  hut  soon  ending 
in  Recovery. — Immediately  after  the  accident  the  patient  is  found  more 
or  less  paralyzed  and  anaesthetic  in  the  lower,  and  occasionally  in  the 
upper  extremities,  but  the  bladder  is  not  usually  affected,  while  im- 
provement begins  in  a  few  days,  and  recovery  is  complete  in  a  few 
weeks  or  months. 

(3)  Severe  Symptoms  at  first.,  followed  hy  a  Protracted  Illness  from 
ivhich  the  Patient  usually  Recovers. — Soon  after  the  accident  the 
patient  complains  of  a  motor  Aveakness,  which  gradually  increases  until 
the  extremities  are  paralyzed.  He  also  complains  of  pains  in  the  back 
of  the  neck,  loins,  or  along  the  vertebral  column,  which  is  often  exces- 
sively sensitive  and  tender  to  pressure,  and  various  parsesthesise,  but 
aneesthesia  is  not  well  marked.  Vomiting  and  loss  of  consciousness 
may  be  present  at  first,  the  extremities  are  cold  and  livid,  and  occasion- 


COXCUSSION    OF    THE    SPIXAL    CORD.  597 

ally  there  is  retention  of  urine,  while  patients  often  manifest  a  high 
degree  of  mental  irritability  for  a  long  time.  Gradual  improvement 
now  occurs,  but  the  patient  complains  of  great  weakness,  and  even 
slight  atrophy  of  some  of  the  muscles  may  occur,  and  complete  recovery 
from  the  paralysis  may  not  take  place  for  several  years,  while  patients 
may  remain  irritable  and  sensitive  long  after  all  the  paralytic  symptoms 
have  disappeared. 

(4)  Very  Slight  Symptoms  at  first,  but  subsequently  a  Severe  Pro- 
gressive Spinal  IHsease  develops,  and  the  result  is  doubtful. — This 
form  of  concussion  is  usually  caused  by  railway  collisions,  and  immedi- 
atel}'  after  the  injury  the  symptoms  are  insignificant.  At  first,  indeed, 
the  patient  is  unusually  calm  and  self  possessed,  and  he  may  busy  him- 
self for  some  hours  in  assisting  his  less-fortunate  fellow  sufferers,  but 
on  reaching  home  he  becomes  talkative  and  excited,  and  is  now  apt  to 
burst  into  tears.  On  the  following  day  he  complains  of  feeling  shaken 
or  bruised  all  over,  but  it  is  not  until  the  lapse  of  from  a  few  days  to  a 
week  or  more  that  he  finds  himself  unfit  for  exertion  and  unable  to 
attend  to  business.  When  the  patient  is  examined  some  Aveeks  after 
the  injury,  the  back  is  found  painful  on  movement;  some  of  the  spinous 
processes  are  found  tender  on  presure;  the  patient  holds  himself  stiff" 
and  erect  in  walking,  as  if  the  various  vertebrae  were  soldered  into  one 
piece,  and  he  is  unable  to  bend  forwards  to  pick  anything  off"  the 
ground,  to  move  the  spine  backwards  or  laterally,  or  to  raise  himself 
from  the  horizontal  position  without  the  aid  of  bis  hands.  Girdle  sen- 
sations, parresthesiee  of  all  sorts,  and  anaesthesia  or  hyperesthesia  in 
varying  degrees  and  in  diff"erent  situations  may  be  present,  while  weak- 
ness of  the  bladder  and  diminution  of  the  sexual  power  are  frequently 
observed.  After  a  time  marked  atrophy  may  take  place  in  individual 
muscles  and  groups  of  muscles,  and  at  times  it  may  be  extensively  dis- 
tributed. The  extremities  are  cold  and  bluish,  the  general  nutrition  is 
impaired,  and  the  expression  of  the  countenance  changes  to  one  indi- 
cating great  anxietv  and  nervousness.  Patients  often  suff'er  from 
muscse  volitantes  and  spectral  images,  intolerance  of  light,  or  diplopia 
and  strabismus,  while  they  are  often  annoyed  by  deafness,  noises  in  the 
ears,  or  great  intolerance  of  sound.  The  patient  is  irritable  and  timid, 
suffers  from  a  feeling  of  constriction  in  the  head,  sleeplessness,  con- 
fusion of  thoughts,  weakness  of  memory  and  intelligence,  impaired 
power  of  work,  and  his  friends  observe  that  his  whole  character  has 
undergone  a  serious  change.  In  cases  of  this  kind  the  patient  may  die 
from  bedsores  and  pypemia,  become  permanently  paralyzed  in  the  lower 
extremities,  or  gradually  recover. 


598      SHOCK,  CONCUSSION,    AND    ALLIED    CONDITIONS. 

III.  CONCUSSION   OF   THE    BKAIN. 

Etiology. — The  exciting  causes  of  cerebral  concussion  are  severe 
injuries,  such  as  falls  from  a  height  or  blows  on  the  head,  which  cause 
the  whole  mass  of  the  brain  to  be  jolted  or  shaken.  Concussion  may 
be  complicated  by  fracture  of  the  skull,  and  in  such  cases  the  effects  of 
the  concussion  are  often  less  severe  than  in  uncomplicated  cases,  ap- 
parently because  a  certain  amount  of  the  applied  force  is  expended  in 
producing  the  fracture. 

Symptoms. — Concussion  is  a  special  form  of  shock  and  its  s^'mptoms 
may  be  described  under  four  stages  :  (1)  the  stage  of  collapse;  (2)  the 
stage  of  rallying  or  vomiting ;  (8)  the  stage  of  reaction;  and  (4)  the 
stage  of  gradual  convalescence. 

(1)  The  Stage  of  Collapse.  The  symptoms  of  this  stage  are  some- 
what variable.  In  the  slighter  forms  the  patient  suffers  from  transient 
confusion  of  ideas,  and  slight  giddiness.  He  may  feel  weak  and  faint 
and  be  unable  to  maintain  the  erect  posture.  In  the  more  severe  forms 
the  symptoms  are  those  of  collapse,  with  loss  of  consciousness ;  but 
paralysis,  such  as  occurs  in  comi)ression  of  the  brain,  is  never  present. 
The  patient  is  semi-conscious  or  insensible,  most  reflex  actions  are 
abolished,  the  skin  is  cold  and  pallid,  the  respirations  superficial  and 
shallow,  the  pulse  feeble  or  imperceptible  at  the  wrist,  whilst  the  pupils 
may  either  be  contracted,  dilated,  or  unequal. 

(2)  The  Stage  of  Rallying  or  of  Vomiting.  After  a  period  varying 
from  a  few  minutes  even  up  to  days,  according  to  the  severity  of  the 
attack,  the  patient  usually  begins  to  show  signs  of  rallying.  This  stage 
is  often  ushered  in  by  vomiting,  or  very  occasionally  by  an  e})ileptiform 
attack ;  the  pulse  improves  in  strength,  the  respirations  become  less 
shallow  and  more  perceptible,  the  body  becomes  warmer,  reflex  actions 
can  be  excited,  and  the  patient  gives  evidence  of  returning  sensil>ility, 
while  he  may  exhibit  signs  of  mental  distress. 

(3)  The  Stage  of  Reaction.  The  symptoms  of  the  stage  of  rallying 
are  succeeded  by  those  of  reaction.  In  this  stage  the  phenomena  of 
febrile  reaction  manifest  themselves  by  the  usual  symptoms — hot  and 
dry  skin,  quick  and  hard  pulse,  and  scanty  urine  ;  while  the  patient  is 
drowsy,  yet  quite  conscious  when  roused  by  a  question  addressed  to  him. 

In  some  cases  these  symptoms  gradually  develop  into  those  of  com- 
pression and  the  patient  dies  comatose,  while  in  other  cases  the  symp- 
toms of  reaction  give  place  to  those  of  inflammation  of  the  brain.  This 
stage  may  continue  from  three  to  twelve  days  in  cases  which  recover. 

(4)  The  Stage  of  Convalescence.     Reaction  is  followed  by  a  pro- 


CONTUSION    OF    THE    BRAIX.  599 

gressive  subsidence  of  the  symptoms,  and  either  by  a  gradual  restora- 
tion of  the  patient  to  health,  or  the  establishment  of  one  or  other  of 
several  chronic  affections  of  the  nervous  system. 

Cerebral  Irritation. — In  another  form  of  nervous  disturbance  follow- 
ing injuries  of  the  head,  and  described  by  Erichsen  under  the  name  of 
cerebral  irritation,  the  phenomena  of  cerebral  excitement  are  associated 
with  those  of  loss  of  function.  The  patient  assumes  a  peculiar  attitude : 
he  lies  with  the  body  bent  forwards,  the  knees  drawn  up  on  the  abdomen, 
the  legs  bent  on  the  thighs,  the  forearms  flexed  on  the  arms,  and  the 
hands  drawn.  The  patient  is  restless,  and  frequently  changes  his  posi- 
tion, but  never  stretches  himself  out  or  assumes  the  supine  posture. 
The  eyelids  are  firmly  closed :  the  pupils  are  contracted :  the  surface 
of  the  body  is  pale  and  cold  ;  and  the  pulse  is  small,  feeble,  and  slow, 
being  seldom  more  than  seventy  beats  per  minute.  The  sphincters 
remain,  as  a  rule,  unaffected. 

The  patient  is  indifferent  to  everything  around  him,  and  is  only 
partially  conscious.  He  may,  however,  be  roused  when  addressed  in  a 
loud  voice,  and  then  looks  up,  mutters  indistinctly,  or  frowns  and  turns 
hastily  away.     His  sleep  is  not  stertorous. 

After  a  period  of  from  one  to  three  weeks  the  pulse  improves,  the 
body  becomes  warmer,  the  flexed  attitude  is  abandoned,  and  the  mental 
irritability  gives  place  to  mental  feebleness  and  torpidity. 

The  course  of  concussion  is  variable.  Some  patients  die  during  the 
stage  of  collapse,  and  others  from  compression  or  encephalitis  following 
an  excessive  reaction.  Even  after  apparent  recovery  the  patient  often 
suffers  from  persistent  headache  ;  his  mental  powers  are  impaired  :  his 
speech  may  be  indistinct  and  stuttering,  his  special  senses  may  be  per- 
manently impaired  ;  and  he  remains  excitable  and  is  apt  to  give  way  to 
uncontrollable  bursts  of  passion. 

IV.  CONTUSION    OF   THE    BEAIN. 

Whenever  the  skull  undergoes  a  change  of  form  as  the  result  of  injury 
the  substance  of  the  brain  may  be  contused  or  lacerated.  The  contusion 
may  be  situated  immediately  beneath  the  portion  of  the  skull  where  the 
injury  was  inflicted,  or  on  the  opposite  side  of  the  brain  as  the  result 
of  contrecoup,  or  both  these  places  may  be  simultaneously  affected. 

The  symptoms  of  contusion  are  always  complicated  by  those  of  con- 
cussion and  of  compression.  The  diagnosis  of  contusion  must  be  made 
by  the  presence,  in  addition  to  the  symptoms  caused  by  a  general 
injury  to  the  brain,  of  ]ihenomena  like  monospasms  or  monoplegia  which 
indicate  a  local  lesion  in  the  absence  of  any  signs  of  fi-acture  of  the  skull. 


600    SHOCK,  coxcussioN,  AjSTd  allied  conditions. 


V.  COMPRESSION   OF  THE    BRAIN. 

Compression  of  the  brain  may  occur  after  injuries  from  the  pressure 
of  a  fractured  portion  of  the  bones  of  the  skull,  the  presence  of  ex- 
travasated  blood,  pus  formed  within  the  skull,  or  of  a  foreign  body 
lodged  there. 

The  patient  becomes  unconscious,  the  l)reathing  is  slow,  deep,  ?^nd 
stertorous,  wliile  the  cheeks  are  puffed  out  during  respiration.  The 
surface  of  the  body  is  cool  at  first,  but  soon  becomes  hot  and  bathed  in 
perspiration.  The  pupils  are  dilated  or  unequal,  the  pulse  is  slow  and 
full,  the  feces  pass  involuntariW,  and  there  is  retention  of  urine.  This 
condition  of  stupor  sometimes  alternates  with  paroxysms  of  delirium, 
while  local  spasms  or  j^aralyses  are  sometimes  observed,  but  it  is  prob- 
able that  in  these  cases  the  motor  area  of  the  cortex  is  not  often  lacerated 
or  contused. 

For  further  information  with  regard  to  contusion  and  compression  of 
the  brain  the  reader  is  referred  to  surgical  works. 

Morbid  Anatomy. — In  shock  all  the  cavities  of  the  heart  are  usually 
distended  with  blood  and  the  veins  of  the  body,  especially  tlie  abdominal 
veins,  are  engorged.  No  changes  have  been  discovered  in  the  nervous 
system.  In  cases  of  concussion  which  have  terminated  fatally  at  an 
early  period,  small  extravasations  of  blood  have  been  found,  in  the  spinal 
variety,  in  the  cord  and  its  membranes ;  and  in  the  cerebral  variety,  in 
the  brain  and  its  membranes.  In  rapidly  fatal  cases  of  spinal  concussion, 
fractures  of  the  vertebrae,  laceration  of  the  membranes,  or  meningeal 
or  spinal  hemorrhage  have  been  observed,  Avhile  in  the  cerebral  variety 
the  morbid  changes  discovered  consist  of  superficial  lacerations,  minute 
hemorrhagic  extravasations  either  studded  on  the  surface  of  the  brain  or 
in  its  substance,  and  occasionally  of  a  difiiised  ecchymosis  of  the  pia 
mater.  In  cases  of  spinal  concussion  which  give  rise  to  a  protracted 
illness  or  to  progressive  spinal  disease  the  symptoms  are  caused  by 
secondary  meningo-myelitis.  It  is  probable  that  death  is  caused  suddenly 
in  some  cases  of  cerebral  concussion  from  injury  of  the  roots  of  the 
pneumogastric  nerves. 

In  contusion  of  the  brain  capillary  hemorrliagic  extravasations  have 
been  found  either  limited  to  the  cortex  or  diff"used  through  the  substance 
of  the  brain.  When  the  injury  is  localized  the  extravasations  may  be 
so  closely  aggregated  that  the  part  aff"ected  presents  the  appearance  of 
a  hemorrhagic  infarction.  The  extravasations  are  more  diffused  when 
the  substance  of  the  brain  is  contused.     Compression  of  the  brain  is 


COMPRESSION    OF    THE    BRAIX.  (501 

caused  by  depressed  fractures,  extravasated  blood,  tbe  formation  of  pus, 
or  the  lodgement  of  a  foreign  l^ody  within  the  cavity  of  the  skull. 

3Iorhid  Physiology. — The  most  striking  phenomena  of  shock  are 
those  which  cluster  around  the  organs  of  circulation.  The  experi- 
ments of  Goltz  and  Brunton  show  that  shock  results  probably  from 
cardiac  paralysis  combined  with  vaso-motor  paralysis  of  the  laroe  vas- 
cular trunks  of  the  abdomen.  Brunton  states  that  moderate  blows  on 
the  abdomen  of  frogs  produce  in  some  stoppage  of  the  heart  without 
dijatation  of  the  abdominal  vessels,  and  in  others  vascular  dilatation 
without  arrest  of  the  cardiac  pulsations,  while  severe  blows  produce 
both  effects  simultaneously.  The  vessels  of  the  alxlomen  are  so  large 
that  when  fully  relaxed  they  are  capable  of  containing  almost  all  the 
blood  in  the  body,  and  consequently  the  condition  resulting  from  this 
rapid  dilatation  is  equivalent  to  a  sudden  hemorrhage.  This  double 
condition  of  cardiac  failure  and  vascular  dilatation  produces  amemia  of 
the  nerve  centres,  and  this  accounts  for  the  pallor  and  coldness  of  the 
surface  of  the  body,  and  the  w^eak,  compressible,  and  fluttering  pulse. 
It  must  not,  however,  be  forgotten  that  the  injury  which  has  disordered 
the  functions  of  the  cardiac  and  vaso-motor  centres  in  the  medulla 
oblongata  must  also  have  produced  a  directly  deleterious  effect  upon 
the  nerve  centres.  The  disorders  of  respiration,  the  cries  of  pain,  and 
the  various  bodily  contortions  which  are  caused  by  bodily  injuries  or 
severe  mental  excitement  show  that  excessive  stimuli  occasion  powerful 
outgoing  discharges  from  the  higher  nerve  centres.  But  a  powerful 
discharge  from  a  nerve  centre  is  followed  by  temporary  impairment  or 
abolition  of  its  functions,  and  it  is  probable  that  the  arrest  of  the  func- 
tions of  the  higher  nerve  centres,  caused  by  the  application  of  a  sudden 
and  powerful  stimulus,  is  the  most  important  factor  in  the  production 
of  the  phenomena  of  shock.  The  symptoms  of  erethismic  shock  may 
be  explained  partly  on  the  supposition  that  the  nervous  tissues  are  in 
the  irritable  condition  frequently  observed  when  they  are  imperfectly 
nourished,  and  partly  on  the  supposition  that  the  phenomena  of  excite- 
ment are  in  great  part  due  to  the  abolition  of  the  functions  of  the 
higher  nerve  centres,  thus  permitting  a  greater  activity  of  the  loAver 
nerve  centres  to  take  place. 

The  symptoms  of  spinal  and  cerebral  concussion  have  both  been 
attributed  by  one  set  of  authorities  to  vascular  spasm,  and  by  others  to 
vascular  paralysis,  but  they  are  most  probably  caused  by  molecular  dis- 
turbance of  the  gray  matter  of  the  spinal  cord  and  brain  respectively, 
which  is  of  such  a  character  that  it  is  attended  by  impairment  or  loss  of 
the  functions  of  the  nerve  cells  and  fibres.  In  contusion  of  the  brain 
the  part  that  is  the  chief  centre  of  the  injury  is  more  or  less  permanently 


602      SHOCK,  CONCUSSION,   AND    ALLIED    CONDITIONS. 

damaged  and  its  functions  destroyed,  while  a  widely  diffused  molecular 
disturbance  occurs  in  the  remaining  parts  of  the  brain.  In  compres- 
sion of  the  brain  the  functions  of  the  organ  are  abolished  partly  because 
the  whole  brain  is  rendered  antemic  by  the  pressure  to  which  the  organ 
is  subjected  owing  to  the  diminution  of  the  cranial  cavity,  and  partly 
by  the  molecular  disturbance  produced  by  the  suddenness  of  the  injury. 

Treatment. — The  great  aim  of  treatment  is  to  excite  reaction,  but  it 
must  be  borne  in  mind  tliat  when  once  reaction  appears  it  is  apt  to 
become  excessive.  If  the  threatened  arrest  of  the  heart's  action  is  of 
purely  nervous  origin,  Savery  recommends  that  blood  should  be  imme- 
diately drawn  from  the  external  jugular  vein,  but  if  it  be  caused  by 
hemorrhage  then  transfusion  of  l)l()od  appears  to  afford  the  best  chance 
of  success.  In  every  case  of  shock  the  patient  should  be  well  Avrapped 
up  in  warm  blankets  and  surrounded  by  hot  bottles.  Stimulants  must 
now  be  given  internally,  brandy  being  generally  the  readiest  and  best. 
If  the  patient  be  unable  to  swallow,  ammonia  or  ether  may  be  injected 
subcutaneously  or  into  a  vein,  or  a  stimulating  enema  may  be  given. 
Tincture  of  digitalis  may  be  administered  in  half  drachm  doses,  but  its 
action  is  too  slow  to  be  of  much  use  in  urgent  cases. 

The  treatment  of  concussion  consists  of  absolute  and  prolonged  rest. 
One  of  the  most  important  rules  of  treatment  is  to  abstain  from  giving 
stimulants  during  the  stage  of  collapse  except  in  unusually  severe  cases. 
In  this  stage  the  patient  should  be  surrounded  by  warm  blankets  and 
hot  bottles,  and  absolute  rest  in  a  dai'kened  room  should  be  enjoined 
until  the  stage  of  reaction  is  passed.  During  the  stage  of  reaction  a 
moderate  purgative  may  be  given,  and  ice  may  be  applied  to  the  head 
if  agreeable  to  the  patient,  while  the  diet  should  be  plain  and  unstimu- 
lating  consisting  chiefly  of  milk.  Spinal  concussion  must  be  treated 
on  the  same  general  ])rinciples  as  the  cerebral  variety.  The  patient 
should  be  made  to  lie  on  his  face  or  side,  or  on  his  back,  as  recom- 
mended by  Erichsen,  on  a  couch  Avhich  is  tilted  a  little  at  its  foot. 
When  the  case  has  become  chronic  the  usual  remedies  for  meningo- 
myelitis  must  be  employed.  Contusion  and  compression  of  the  brain 
from  external  injury  come  under  the  care  of  the  surgeon. 


CHAPTER    XY. 

VASCULAR  DISEASES  OF  THE  BRAIN. 

I.  AN^^MIA   AND   OCCLUSION  OF  THE   INTRACRANIAL  VESSELS. 

Etiology — Cerebral  ansemia  may  be  divided  into  1,  Mmwers«?  anaemia, 
Avhicli  results  from  the  same  causes  as  anaemia  of  the  body  generally : 
and  2,  partial  anaemia,  which  is  caused  by  obstruction  of  one  of  the 
cerebral  vessels. 

1.  Universal  Cerebral  Anaemia. 

Symptoms. — The  universal  form  of  the  disease  may  be  divided  into 
a,  acute;  and  h,  chronic  universal  cerebral  ana?mia. 

a.  Acute  Universal  Cerebral  Ancemia. — The  initial  symptoms  of  the 
ansemia  which  is  caused  by  severe  hemorrhage,  are  obscuration  of  the 
senses;  buzzing  in  the  ears;  dizziness;  contraction,  followed  by  dilata- 
tion of  the  pupils ;  imperfect  reaction  to  external  stimuli ;  and  loss  of 
consciousness.  The  surface  becomes  cold  and  pale,  the  respiratory 
movements,  accelerated  at  first,  become  slow,  and  this  condition  is  fre- 
quently followed  by  general  convulsions  and  coma.  In  an  ordinary  fam^- 
ing  fit  or  syncope  there  is  at  first  some  degree  of  mental  incoherence 
manifested  by  the  inability  of  the  patient  to  direct  his  attention  to  a 
particular  object,  a  feeling  of  oppression  in  the  chest,  along  with  a  ten- 
dency to  yawn.  The  face  becomes  pale,  a  cold  perspiration  breaks  out 
on  the  forehead  and  sometimes  over  the  entire  body,  and  there  are  gen- 
eral muscular  relaxation,  ringing  in  the  ears,  dimness  of  sight,  nausea, 
and  sometimes  vomiting.  The  pulse  is  small,  compressible,  but  regular. 
The  patient  may  noAV  recover  or  fall  insensible  to  the  ground,  and  after 
a  few  moments  in  the  recumbent  position  he  begins  to  rally. 

h.  Chronic  Universal  Cerebral  Anaemia. — In  these  cases  the  patient 
is  fretful  and  restless,  his  sleep  is  disturbed  by  dreams,  while  he  suffers 
from  intolerance  of  light  and  sound  and  great  mental  irritability.  These 
symptoms  are  frequently  succeeded  by  the  phenomena  of  depression, 
and  sometimes  the  latter  predominate  from  the  first.  The  patient 
suffers  from  almost   constant  headache,  vertigo,   nausea,  and  faintness. 


604  VASCULAR    DISEASES    OF    THE    BRAIN. 

The  pulse  is  small  and  compressible,  the  cardiac  impulse  feeble,  and 
tliere  is  great  disinclination  for  either  mental  or  physical  exertion. 

In  the  severe  forms  of  chronic  or  subacute  cerebral  antemia,  such  as 
that  produced  by  starvation,  or  that  Avhich  arises  during  the  course  of 
exhausting  fevers,  delirium  becomes  a  prominent  symptom.  During 
the  delirium  of  cerebral  anaemia  the  patients  are  excited  and  sometimes 
maniacal;  there  are  illusions  of  sight  and  hearing,  and  delusions  of 
persecution.  The  duration  of  this  condition  is  variable;  it  may  last  a 
few  hours  or  days  only,  but  it  sometimes  continues  for  weeks,  and  occa- 
sionally passes  into  permanent  insanity. 

Cerebral  anaemia  is  seen  in  infants  after  severe  diarrhciea,  or  other 
exhausting  disease  ;  and  as  this  is  the  form  Avhich  was  called  by  Marshall 
Hall  liydroceflialoid  or  hydrenccphaloid  disease,  it  demands  special 
notice.  The  affection  may  be  divided  into  two  stages — that  of  irri- 
tability, and  of  torpor.  In  the  first  stage,  the  infant  is  irritable  and 
restless,  with  flushed  face,  Avarm  skin,  and  frequent  pulse  :  the  patient 
starts  on  being  touched  or  on  hearing  any  sudden  noise,  and  sleep  is 
disturbed  and  interrupted  by  sighs,  moans,  or  screams.  During  the 
second  stage  the  countenance  becomes  pale,  the  cheeks  and  extremities 
cold,  the  eyelids  are  half  closed,  the  eyes  sunk  iii  their  sockets,  there  is 
frequently  slight  strabismus,  and  the  pupils  are  dilated  and  do  not  con- 
tract to  light.  The  breathing  is  irregular  and  sighing,  the  voice  husky, 
and  there  is  sometimes  a  teasing  cough  with  rattlini;  in  the  throat.  A 
most  important  symptom  which  distinguishes  this  disease  from  liydro- 
cephalus  is  that  the  fontanelle,  instead  of  being  tense  as  in  tlie  latter 
disease,  is  depressed.  The  child  inclines  almost  constantly  to  fall  into 
a  sleep,  which  may  pass  into  coma  and  death,  but  under  appropriate 
treatment  gradual  recovery  usually  takes  place. 

2.  Partial  Cekeijral  An.emia  (Occlusion  ok  thk  Intracranial 

Vessels). 

Occlusion  of  the  cerebral  vessels  may  take  place  in  a,  the  arteries ; 
h,  the  veins  and  sinuses ;  and  t\  the  capillaries  of  the  brain. 

a.    Occlusion  of  the  Cerebral  Arteries. 

Etiology. — The  arteries  of  the  brain  may  be  occluded  by  a  substance 
carried  from  a  distant  part  of  the  circulation,  constituting  embolism ;  or 
by  a  clot  formed  on  the  spot,  constituting  thrombosis. 

An  embolus  consists  of  a  fibrinous  mass  washed  away  from  the  left 
cavities  of  the  heart,  the  mitral   or   aortic  valves,  or  the   arch  of  the 


AN.EMIA  AND   OCCLUSION   OF   INTRACRANIAL   VESSELS.    605 

aorta.  In  cases  of  cancer  of  the  lungs,  a  nodule  of  the  growth  may 
possibly  be  carried  from  the  pulmonary  veins,  and  pass  into  the  cerebral 
vessels. 

Thrombosis  of  an  artery  occurs  most  frequently  when  the  internal 
surface  of  the  vessel  is  rendered  rough  and  uneven  by  arterial  degenera- 
tion. The  predisposing  causes  of  thrombosis  are  all  those  conditions 
which  tend  to  diminish  the  force  of  the  heart's  action  and  to  alter  the 
<|uality  of  the  blood,  and  thrombosis  is  particularly  liable  to  occur  when 
these  general  causes  and  local  arterial  degeneration  are  conjoined.  Em- 
bolism occurs  most  frequently  in  young,  and  thrombosis  in  old  people. 

Symptoms. — The  symptoms  of  embolism  of  a  cerebral  artery  are 
almost  identical  with  those  of  cerebral  hemorrhage  in  their  mode  of 
onset  and  general  characters,  but  the  unconsciousness  caused  by  embolus 
is,  as  a  rule,  more  transient  than  that  caused  by  hemorrhage.  In  some 
cases  the  patient  is  suddenly  attacked  with  dizziness  and  utters  an  in- 
voluntary cry,  or  complains  momentarily  of  headache  and  immediately 
loses  consciousness,  but  in  other  cases  the  patient  ovAj  complains  of 
dizziness  and  slight  confusion  of  mind  for  a  minute  or  two  and  becomes 
suddenly  paralyzed  and  often  aphasic,  but  without  loss  of  consciousness. 
In  still  other  cases  the  attack  is  ushered  in  by  an  attack  of  convulsions, 
which  may  be  general  like  an  ordinary  epileptic  attack,  or  limited  to 
one-half  or  to  a  part  of  one-half  of  the  body.  When  general  convulsions 
are  present  they  occur  simultaneously  with  the  loss  of  consciousness  and 
are  immediately  followed  by  paralysis,  while  unilateral  and  partial  con- 
vulsions may  recur  repeatedly  before  paralysis  is  fully  established.  In 
many  cases  sudden  speechlessness  constitutes  the  only  symptom  of  em- 
bolus of  a  cerebral  artery  and  in  these  cases  this  symptom  may  disappear 
when  collateral  circulation  is  established,  but,  as  a  rule,  the  aphasia  is 
associated  with  right-sided  hemiplegia.  The  state  of  the  pupils  varies 
during  the  attack. 

The  sympto))is  of  thrombosis  are,  as  a  rule,  more  gradual  in  their 
development  than  those  of  embolus.  The  more  usual  premonitory 
symptoms  of  thrombosis  of  a  cerebral  artery  are  headache,  dizziness,  a 
sense  of  general  confusion,  numbness,  coldness,  or  formication  of  one 
extremity  or  of  one-half  of  the  body,  and  considerable  mental  disturb- 
ance, especially,  marked  loss  of  memory. 

Convulsive  movements  occasionally  precede  the  appearance  of  paral- 
ysis, but,  as  a  rule,  the  loss  of  motor  power  begins  gradually,  and  its 
progress  is  marked  by  successive  remissions  and  exacerbations  until 
ultimately  a  more  or  less  extensive  paresis  is  established.  The  duration 
of  the  prodromal  stage  may  vary  from  a  few  days  to  a  few  months,  and 
occasionally  apoplectic  symptoms  may  come  on  suddenly  as  in  embolism. 


606  VASCULAR    DISEASES    OF    THE    BRAIX. 

When  once  the  vessel  has  become  completely  occluded  the  further  prog- 
ress of  thrombosis  is  like  that  of  embolus  of  a  corresponding  vessel. 

When  softening  occurs  either  from  embolus  or  thrombosis,  the  temper- 
ature, according  to  Bourneville,  begins  to  rise  on  the  second  or  third 
day  of  the  attack  and  in  two  or  three  days  it  may  reach  40°  C.  (104°  F.). 
After  a  few  days  longer  the  temperature  sinks  rapidly,  its  decline  being 
more  rapid  than  after  the  period  of  inflammatory  reaction  in  cases  of 
hemorrhao-e.  When  once  softening  has  become  thoroughly  established 
the  symptoms  are  generally  the  same  as  those  of  other  localized  cerebral 
diseases,  while  the  sensory,  trophic,  and  vaso-motor  disorders,  and  the 
aifections  of  the  special  senses  are  the  same  as  those  occurring  in  cerebral 
hemorrhao-e.  In  some  cases  of  embolism,  however,  the  ophthalmic 
artery  is  occluded,  and  the  patient  l)ecomes  suddenly  blind  on  that  side, 
while  an  ophthalmoscopic  examination  reveals  the  usual  signs  which 
indicate  occlusion  of  the  central  artery  of  the  retina. 

In  cases  of  embolism  the  signs  of  valvular  disease  of  the  heart  or  of 
disease  of  the  large  arteries  are  detected  on  physical  examination,  and 
in  cases  of  thrombosis  the  signs  of  degeneration  of  the  arteries  are 
present. 

In  some  cases  of  occlusion  of  cerebral  arteries  the  symptoms  begin  to 
improve  at  an  early  period  and  the  patient  may  ultimately  recover  com- 
pletely. In  these  cases  it  is  evident  that  collateral  circulation  has 
become  established  before  softening  has  taken  place.  In  cases  in  which 
recovery  has  taken  place  the  patient  is  liable  to  be  suddenly  attacked 
by  occlusion  of  other  vessels. 

h.   Thrombosis  of  the  Cerebral  Sinuses. 

Etiology. — Thrombosis  is  prone  to  occur  in  the  cerebral  sinuses 
because  they  are  traversed  by  bands  of  connective  tissue,  are  destitute 
of  muscular  walls,  and  are  rigid  tubes  incapable  of  collapsing.  Throm- 
bosis of  the  sinuses  is  particularly  liable  to  occur  in  infants  during  the 
collapse  induced  by  severe  diarrhoea,  while  in  adults  it  occurs  in  cases 
of  profuse  sujjpuration,  cancer,  senile  marasmus,  and  other  diseases 
associated  with  great  debility.  In  other  cases  inflammation  of  the 
sinuses  is  produced  by  disease  or  injury  of  the  cranial  bones,  which  is 
followed  by  the  formation  of  purulent  thrombi.  Erysipelas  of  the  head 
and  face,  furunculus  of  the  face,  and  purulent  inflammation  of  the  deep 
muscles  of  the  neck,  are  other  causes  of  thrombosis  of  the  sinuses. 

Symptoms. — The  symptoms  of  thrombosis  of  the  sinuses  in  children 
consist  of  convulsions  or  paralysis  in  addition  to  the  collapse,  and  som- 
nolence caused  bv  the  cerebral  anaemia  which  results  from  an  exhaust- 


AX.EMIA  AXD  OCCLUSIOX   OF   IXTRACRAXIAL   VESSELS.    607 

ing  diarrhoea.  The  motor  symptoms  most  commonly  observed  are 
rigidity  of  the  muscles  of  the  neck  and  sometimes  also  of  those  of  the 
limbs,  nystagmus,  strabismus,  ptosis,  and  paresis  of  the  facial  muscles. 
The  fontanelles  are  at  first  depressed  as  in  the  hydrencephaloid  disease 
described  by  Marshall  Hall,  but  as  the  disease  advances  either  effusion 
of  serum  or  extensive  meningeal  or  intra-cerebral  hemorrhages  may 
take  place  and  the  fontanelles  become  less  tense  and  the  cranial  bones 
pushed  apart. 

Thrombosis  of  the  sinuses  from  marasmus  in  adults  give  rise  to  very 
indefinite  symptoms,  and  at  times  a  slight  degree  of  apathy  and  general 
depression  are  the  only  symptoms  present.  At  the  outset  the  patient 
may  complain  of  headache,  nausea,  and  vomiting,  but  these  soon  give 
place  to  coma,  and  in  a  few  cases  loss  of  consciousness  is  preceded  by 
delirium,  which  occasionally  assumes  a  maniacal  character.  The  most 
usual  motor  disturbances  are  strabismus,  trismus,  tremors  and  con- 
tractures, epileptiform  convulsions,  or  paralysis,  which  may  involve  one- 
half  or  both  sides  of  the  body.  At  other  times  paralysis  and  contrac- 
tures may  be  associated,  one  extremity  being  the  seat  of  contractui-e 
and  the  other  of  paralysis.  Swelling  of  the  veins  outside  the  skull 
affords  a  valuable  sign  of  thrombosis  of  the  sinuses.  The  superior 
longitudinal  sinus  communicates  directly  with  the  veins  of  the  nasal 
cavities  and  with  those  on  the  upper  surface  of  the  skull,  and  conse- 
quently thrombosis  of  it  may  give  rise  to  epistaxis,  or  to  distention  of 
the  veins  which  run  from  the  temples  on  both  sides  to  the  anterior  fon- 
tanelle,  and  there  may  also  be  cyanosis  of  that  part  of  the  face  which 
is  supplied  by  the  anterior  facial  veins. 

The  lateral  sinus  communicates  with  a  small  vein  which  traverses 
the  mastoid  process,  and  in  thrombosis  of  the  sinus  localized  oedema 
behind  the  ear  occasionally  may  make  its  appearance.  Simultaneous 
thrombosis  of  both  lateral  sinuses  gives  rise  to  the  same  symptoms  as 
occlusion  of  the  superior  longitudinal  sinus. 

The  cavernous  sinus  communicates  with  the  ophthalmic  vein,  and  in 
thrombosis  of  the  sinus,  venous  hypersemia  of  the  fundus  oculi  has  been 
observed,  along  with  cedema  of  the  eyelids  and  conjunctiva,  and  promi- 
nence of  the  eyeball  caused  by  congestion  of  the  retrobulbar  frontal 
veins.  Interference  with  the  nutrition  of  the  nerves  which  pass  along 
the  floor  of  the  sinus  may  also  give  rise  to  paralysis  of  the  oculo-motor 
nerves,  trigeminal  neuralgia,  and  neuroparalytic  ophthalmia. 

The  phlehitie  variety  is  generally  complicated  with  meningitis  and 
cerebral  abscess,  and  it  is  not,  therefore,  always  possible  to  distinguish 
between  the  symptoms  caused  by  each  of  these  morbid  conditions.  In 
the  few  cases  in  which  suppurative  thrombosis  was  alone  present,  the 


608  VASCULAK    DISEASES    OF    THE    BRAIN. 

symptoms  Avere  the  same  as  those  of  septiciiemia  with  pronounced  cere- 
bral symptoms.  The  attack  generally  begins  with  chilliness,  which 
recurs  repeatedly  during  the  course  of  the  disease,  and  the  jiatient 
has  a  characteristic  typhoid  look,  with  dry  tongue,  loss  of  appetite,  and 
mental  confusion.  After  a  time  the  patient  flills  into  a  somnolent  con- 
dition which  gives  place  to  coma,  which  soon  terminates  fatally.  Wlien 
suppurative  thrombosis  is  complicated  with  meningitis,  more  pronounced 
sensory  and  motor  symptoms  are  present,  consisting  of  headache,  hyper- 
algesia, paresis,  paralysis,  or  convulsions.  The  disease  sometimes 
pursues  a  latent  course,  and  is  only  discovered  after  death. 

c.   Occlusion  of  the  Cerebral  (Japillaries. 

Etiology. — In  severe  cases  of  intermittent  fever  the  cerebral  capillaries 
are  liable  to  be  obstructed  by  dark  colored  masses  which  have  been  called 
'pigment  embolism.  The  cerebral  capilhiries  may  also  be  obstructed  by 
oil  globules,  constituting  fat  embolism.  The  cerebral  capillaries  are 
said  to  be  sometimes  occluded  by  linie  Ijccoming  deposited  on  tlieir  walls, 
a  process  named  by  Virchow  lime  metustasis.  (Japillary  embolism  is  sup- 
posed to  give  rise  to  chorea,  but  this  subject  will  be  discussed  hereafter. 

Synqotoms. — If  the  embolic  masses  are  few  in  number  they  do  not 
give  rise  to  symj)tonis  which  can  be  recognized  during  life,  but  if  a  con- 
siderable part  of  the  brain  is  deprived  of  its  nourishment  the  patient 
suffers  from  dift'used  cerebral  symjitoms  such  as  dizziness,  headache, 
nausea,  trembling,  Aveakness  of  the  extremities,  and  loss  of  memory 
with  other  signs  of  mental  decay.  If  the  circulation  is  suddenly 
arrested  in  a  large  portion  of  the  brain  the  symptoms  of  a  localized 
destructive  disease  of  the  cerebrum  may  be  produced. 

Morbid  Anatomy. — Capillary  occlusion  can  only  be  discovered  with 
the  aid  of  the  microscope.  The  first  effect  of  these  emboli  is  to  cause 
anoemia,  and  subsequently  the  various  stages  of  necrobiosis  up  to  com- 
plete softening  are  produced. 

Treatment. — The  treatment  will  depend  upon  the  cause  of  the  emboli 
and  must  be  conducted  on  general  principles. 


II.  CONGESTION    OF   THE    BKAIN. 

Etiology. — Congestion  of  the  brain  may  be  either  active  or  passive, 
and  is  produced  by  the  same  general  causes  as  congestion  of  other 
organs.  It  is,  indeed,  asserted  by  Moxon  that  congestion  of  the  brain 
does  not  give  rise  to  symptoms  which  can  be  set  up  as  a  distinct  disease. 


CONGESTION    OF    THE    BRAIN.  609 

but  apoplectiform  attacks  occur  in  the  course  of  such  diseases  as  loco- 
motor ataxia,  general  pai-alysis,  and  sclerosis  in  patches,  for  which  it  is 
difficult  to  assign  any  other  cause  than  congestion,  and  although  it  is 
probable  that  congestion  has  been  often  assumed  to  exist  without  due 
warrant,  Ave  do  not  feel  ourselves  justified  in  rejecting  the  condition  as 
a  cause  of  a  distinct  and  separate  disease. 

Symptoms. — Congestion  of  the  brain  gives  rise  to  symptoms  which 
vary  widely  in  different  cases,  but  for  clinical  purposes  three  varieties 
may  be  described:  (a)  the  slight,  {h)  the  severe,  and  (c)  the  apoplectic 
form. 

(a)  In  the  slifiht  form  of  congestion  the  prominent  symptoms  are 
sensory  disorders.  The  patient  complains  of  severe  headache,  either 
deep-seated  or  lancinating,  aggravated  by  movement,  light,  sound,  or 
heat,  while  all  intellectual  efforts  become  impossible.  Patients  at  the 
same  time  complain  of  dizziness,  tinnitus  aurium,  and  optical  illusions. 
Sleeplessness  is  an  early  and  important  symptom.  It  is  accompanied 
by  restlessness  and  agitation,  and  if  sleep  do  supervene,  it  is  disturbed 
by  horrible  dreams,  and  the  patient  awakes  unrefreshed  without  relief 
to  the  headache. 

In  venous  hypersemia  the  phenomena  of  mental  depression  are  usually 
more  marked  than  those  of  excitement.  There  is  a  dull  sense  of  oppres- 
sion in  the  head,  the  face  is  livid,  there  is  mental  torpor  with  a  ten- 
dency to  sleep,  and  a  certain  amount  of  confusion  of  ideas,  especially 
on  awaking  after  a  short  sleep. 

(h)  In  the  severe  forms  other  symptoms  are  added.  The  patient 
suffers  so  much  from  vertigo  that  he  is  unable  to  maintain  the  erect 
posture,  and  sudden  vomiting  may  occur  in  the  absence  of  any  gastric 
irritation  to  account  for  it.  The  pulse  is  slow,  full,  and  hard;  the 
arteries  of  the  head  and  neck  beat  forcibly;  the  face  is  frequently, 
although  not  always  flushed,  and  may  at  times  be  livid,  while  a  sensa- 
tion of  flying  heat  shoots  over  the  head  and  neck.  The  pupils  are 
generally  contracted,  and  there  is  some  degree  of  intolerance  of  light 
and  sound.  The  patient  complains  of  intense  headache,  and  is  the 
subject  of  hallucinations  and  illusions  which  pervert  the  judgment, 
and  may  lead  to  strange  and  disorderly  acts.  He  sometimes  endeavors 
to  quit  his  bed,  and  to  pursue  or  run  away  from  imaginary  objects;  he 
is  loquacious  or  bursts  into  a  flood  of  tears,  and  struggles  with  and  tries 
to  escape  from  his  attendants.  After  some  hours  of  excitement  and 
struggling  the  skin  becomes  covered  with  sweat,  the  pulse  is  accelerated, 
the  face  of  a  deep  red  color,  and  the  patient  presents  the  leading  symp- 
toms of  encephalitis;  the  thermometer  shows  that  the  temperature,  if  at 
all  altered,   is   only  slightly   above  the  normal.     If  these    symptoms 

39 


610  VASCULAR    DISEASES    OF    THE    BRAIX. 

persist  for  some  time,  the  phenomena  of  excitement  are  succeeded  by 
those  of  depression,  the  delirium  gradually  gives  place  to  mental 
torpor,  the  muscular  agitation  is  replaced  by  muscular  relaxation,  the 
respiration  becomes  stertorous,  there  are  involuntary  evacuations,  and 
the  patient  falls  into  a  state  of  coma.  An  abundant  secretion  from  the 
conjunctivae  and  mucous  membrane  of  the  mouth  is  said  to  be  a  frequent 
symptom  of  congestion  of  the  brain  in  old  people.  It  is  very  probable 
that  many  of  the  cases  which  have  been  described  as  examples  of  cere- 
bral congestion  ought  to  be  regarded  as  the  delirium  or  mania  which 
so  frequently  follows  a  slight  epileptic  attack. 

The  symptoms  of  cerebral  congestion  in  infancy  are  somewhat  simi- 
lar to  those  of  meningitis.  Both  are  attended  with  partial  or  general 
convulsions,  headache,  contraction  of  the  pupils,  vomiting,  and  consti- 
pation. The  course  of  the  two  affections,  however,  enables  them  to  be 
readily  distinguished.  In  congestion  the  child  has  been  in  good  health 
up  to  the  beginning  of  the  attack,  there  is  little  or  no  elevation  of  tem- 
perature, and  the  disease  terminates  in  recovery  in  two  or  three  days 
at  most. 

(e)  The  ajyojjlectic  form  is  characterized  by  sudden  and  total  loss  of 
consciousness  and  complete  resolution  of  the  limbs,  but  reflex  excita- 
bility is  preserved.  The  patient  recovers  consciousness  in  a  few  hours, 
and  after  a  short  time — two  or  three  days  at  most,  all  the  symptoms 
disappear  without  leaving  a  trace  behind.  Sometimes,  however,  after 
complete  restoration  to  consciousness,  a  certain  amount  of  muscular 
paralysis  remains  in  one  limb,  or  it  assumes  the  hemiplegic  form  and 
persists  for  some  time.  Apoplectiform  attacks  of  this  kind  are  liable 
to  occur  in  the  course  of  locomotor  ataxia,  sclerosis  in  patches,  and 
general  paralysis  of  the  insane.  Patients  suffering  from  these  diseases 
are  sometimes  seized  with  general  convulsions  and  die  comatose  in  a 
fcAV  hours,  and  at  the  autopsy  no  coarse  lesion  of  any  kind  is  discovered 
in  the  brain. 

III.  INTRACRANIAL  HEMORRHAGE. 

Intracranial  hemorrhage  may  be  divided  into  1,  cerebral;  and 
2,  meningeal  hemorrhage. 


1.  Cerebral  Hemorrhage  (Apoplexy). 

Etiology. — Some  families  exhibit  a  predisposition  to  cerebral  hemor- 
rhage, but  this  tendency  is  only  an  indirect  result  of  an  inherited  ten- 
dency to  a  general  arterial  degeneration.     Cerebral  hemorrhage  is  rare 


IXTEACRANIAL    HEMORRHAGE.  611 

before  the  fortieth  year  of  age,  and  it  occurs  more  frequently  in  men 
than  in  women,  but  age,  sex,  as  well  as  occupation  and  climate,  seem 
to  predispose  to  it  only  in  so  far  as  they  tend  to  induce  degeneration  of 
vessels.  The  chief  circumstances  which  predispose  to  cerebral  hemor- 
rhage are  (1)  diseases  of  the  bloodvessels,  (2)  increase  of  the  arterial 
tension,  (3)  disease  of  the  tissues  surrounding  the  vessels,  and  (4)  cer- 
tain diseases  of  the  blood. 

(1)  Diseases  of  the  Vessels. — The  great  majority  of  massive  hemor- 
rhages into  the  substance  of  the  brain  are  due  to  degeneration  of  those 
branches  of  the  Sylvian  artery  which  pass  through  the  anterior  perforated 
space  to  reach  the  corpus  striatum.  By  far  the  most  frequent  cause  of 
intracerebral  hemorrhage  is  that  condition  of  the  arterioles  which  has 
been  described  by  Charcot  and  Bouchard  as  miliary  aneurisms.  These 
aneurisms  are  of  a  reddish  color,  and  vary  from  the  size  of  a  millet 
seed  to  that  of  a  pin's  head.  Sometimes  a  few  only  are  found  in  the 
neighborhood  of  the  ruptured  vessel,  while  at  other  times  they  are  scat- 
tered in  large  numbers  throughout  the  whole  brain.  The  parts  of  the 
brain  in  which  they  are  situated,  in  the  order  of  decreasing  frequency, 
are  the  lenticular  nucleus,  the  optic  thalami,  the  pons,  the  convolutions, 
the  caudate  nucleus,  the  cerebellum,  the  medulla  oblongata,  the  middle 
peduncles  of  the  cerebellum,  and  the  centrum  ovale.  Miliary  aneu- 
risms result,  according  to  Charcot  and  Bouchard,  from  a  kind  of  arterial 
sclerosis  of  the  nature  of  a  chronic  periarteritis.  Atheroma  of  the 
vessels  may  also  lead  to  aneurisms  of  the  larger  and  medium  sized 
arteries  of  the  brain,  and  although  rupture  of  these  are  apt  to  give  rise 
to  hemorrhages  on  the  surface  of  the  brain,  yet  the  hemorrhage  passes 
into  the  substance  of  the  brain  more  frequently  than  is  generally  sup- 
posed. Atheromatous  degeneration  may  also  cause  hemorrhage  indi- 
rectly by  rendering  the  walls  of  the  larger  vessels  rigid,  so  that  the 
pulse-wave  reaches  the  arterioles  without  being  modified  by  the  normal 
elasticity  of  the  arteries. 

Primary  fatty  degeneration  of  the  cerebral  bloodvessels  occurs  at  all 
ages,  and  Paget  believes  that  it  sometimes  predisposes  to  cerebral  hem- 
orrhage in  young  people. 

(2)  Vascular  Tension. — It  is  doubtful  whether  increase  of  the  arte- 
rial tension  ever  gives  rise  to  cerebral  hemorrhage  in  the  absence  of 
disease  of  the  vascular  walls,  but  when  arterial  degeneration  is  present 
any  increase  of  tension  becomes  a  powerful  predisposing  cause  of  hem- 
orrhage. Sudden  exposure  to  cold  may  increase  the  arterial  tension 
by  inducing  extensive  contraction  of  the  cutaneous  arteries.  During 
the  winter  months  it  is  very  common  for  individuals  to  be  found  in  a 
comatose  condition   on  the  streets  and  taken  up  by  the  police  on  the 


612  VASCULAR    DISEASES    OF    THE    BRAIX. 

supposition  that  they  are  drunk.  Such  accidents  usually  occur  in  per- 
sons of  middle  age ;  the  breath  may  smell  of  alcohol,  and  the  person 
attacked  may  be  known  to  have  been  drinking  during  the  evening. 
The  evening  has  been  spent  in  a  heated  apartment,  when,  under  the 
conjoined  influence  of  a  high  temperature,  alcohol,  and  emotional  ex- 
citement, the  cutaneous  vessels  have  become  dilated,  the  skin  bathed  in 
perspiration,  and  the  cardiac  action  accelerated.  On  going  out  into  the 
cold  air  the  surface  becomes  suddenly  chilled,  and  the  arterial  tension 
is  rapidly  augmented ;  the  internal  organs  become  gorged  with  blood : 
and  if,  as  is  frequently  the  case,  the  Avails  of  the  cerebral  vessels  are 
weakened  by  disease,  rupture  of  one  of  them  is  apt  to  occur. 

The  hypertrophy  of  the  left  ventricle,  which  takes  place  in  contracted 
kidney,  taken  along  with  arterio-capillary  fibrosis,  which  invariably 
accompanies  it,  is  a  frequent  cause  of  cerebral  hemorrhage. 

(3)  Condition  of  the  Tissues. — The  theory  that  cerebral  hemor- 
rhage is  generally  preceded  by  softening  of  the  cerebral  tissue,  was 
advanced  by  Rochoux,  and  he  gave  to  this  supposed  process  the  name 
of  ramollisseDtent  hemorrhagfpare,  but  it  is  now  generally  admitted  that 
when  the  softening  is  not  caused  by  occlusion  of  vessels,  it  is  secondary 
to  the  hemorrhage. 

(4)  The  State  of  the  Blood. — Cerebral  hemorrhage  has  been  occa- 
sionally observed  in  the  course  of  diseases  of  the  blood,  like  scorlmtus, 
purpura,  chlorosis,  leucocythemia,  pernicious  ansemia,  icterus,  typhoid 
and  other  specific  fevers. 

Symptoms. — An  attack  of  cerebral  hemorrhage  may  begin  suddenly 
Avithout  any  warning,  but  in  many  cases  premonitory  symptoms  are 
present  some  days  or  even  weeks  before  the  actual  onset  of  the  attack. 
The  usual  forerunners  of  an  apoplectic  attack  are  dizziness,  headache, 
ringing  in  the  ears,  muscae  volitantes,  numbness  in  the  hand  or  foot, 
muscular  tAvitchings  of  the  face  or  some  portion  of  the  extremities,  mis- 
takes in  talkino;  or  Avritino;,  vomitincj,  mental  irritabilitv,  and  drowsiness. 
These  symptoms,  either  separately  or  in  various  combinations,  are  to  be 
regarded  as  warnings  of  apoplexy  only  in  old  people,  or  in  middle-aged 
people  Avith  evidences  of  arterial  degeneration.  The  mode  of  onset  of 
an  attack  of  cerebral  hemorrhage  may  be  divided  into  (1)  the  apo])lecti- 
form,  (2)  the  epileptiform,  and  (3)  the  simple  mode  of  onset. 

(1)  Apoplectifoi-m  Onset. — This  mode  of  onset  is  characterized  by 
sudden  loss  of  consciousness  and  resolution  of  the  limbs,  either  Avith 
or  without  warning,  constituting  what  is  popularly  called  apoplexy. 

When  the  apoplectic  attack  is  Avell  marked  the  patient  lies  in  a  state 
of  profound  coma,  and  is  insensible  to  all  kinds  of  stimuli.  The  face 
is  usually  flushed  and   SAvollen,  although   it   may  occasionally  be  pale 


INTRACRANIAL    HEMORRHAGE.  613 

and  clammy;  the  lips  are  livid;  the  head  and  neck  feel  warm  and 
bathed  in  persi)iration ;  the  carotids  and  other  arteries  throb  violently; 
the  eyelids  are  closed;  the  conjunctivae  are  ingested;  the  eyeballs  are 
fixed;  the  pupils  are  sluggish  to  light;  the  respiration  is  usually  deep, 
Avith  or  without  stertor  and  protrusion  of  the  cheeks  during  expiration ; 
the  pulse  is  generally  full  and  slow ;  and  there  is  either  complete  mus- 
cular resolution,  so  that  the  limbs  when  raised  drop  like  inert  bodies, 
or  the  resolution  is  more  marked  on  one  side  of  the  body  than  on  the 
other.  In  the  severer  cases  there  is  not  only  complete  absence  of  vol- 
untary motion,  but  all  reflex  movements  are  lost,  with  the  exception  of 
the  cardiac  and  respiratory  movements  and  those  concerned  in  the 
second  act  of  deglutition.  In  such  cases  the  patient  may  die  after  a 
few  minutes,  a  few  hours,  or  a  few  days.  In  cases  which  are  less  severe 
from  the  first  or  in  which  some  degree  of  recovery  has  taken  place, 
powerful  irritation  causes  reflex  movements,  and  in  still  less  profound 
cases  the  patient,  when  loudly  spoken  to,  raises  his  eyelids  for  a  moment 
or  two,  and  may  even  reply  in  a  monosyllable  when  loudly  pressed  with 
any  question.  In  such  cases  a  difierence  can  be  detected  between  the 
two  halves  of  the  body ;  the  extremities  of  one  side  offer  some  degree 
of  resistance  to  passive  movements,  while  those  of  the  other  side  sink, 
when  unsupported,  like  inert  masses,  and  the  corner  of  the  mouth  is 
lower  on  one  side  than  on  the  other. 

(2)  The  Epileptiform  Onset. — In  this  mode  of  onset  the  patient, 
either  with  or  without  prodromata,  drops  down  insensible  in  a  kind  of 
epileptic  fit,  and  after  a  time  it  is  discovered  that  he  is  paralyzed  on 
one  side  of  the  body.  The  convulsions  may  be  limited  to  one-half  of 
the  body,  and  this  side  is  subsequently  paralyzed ;  but  if  the  convul- 
sions occur  after  paralysis  has  become  established  the  non-paralyzed 
side  is  the  one  which  is  attacked  with  clonic  spasms.  In  some  of  the 
cases  initiated  by  convulsions  the  patient  may  remain  in  a  somewhat 
lethargic  condition,  with  eyes  closed  or  only  half  open,  for  a  period  of 
from  three  to  six  weeks  and  yet  recover,  but  if  deep  coma  continues  for 
forty-eight  hours  the  case  generally  terminates  fatally. 

(3)  Simple  Mode  of  Onset. — In  the  simple  onset  the  patient  may 
suddenly  fall  from  paralysis,  but  without  loss  of  consciousness.  He 
generally  complains  of  a  feeling  of  "  numbness  "  of  the  paralyzed  side, 
but  does  not  suffer  pain. 

The  temperature  is  lowered  immediately  after  an  apoplectic  attack, 
reaching  in  some  cases  96.5°  F.,  and  in  the  fulminating  foi'ms  it  remains 
low  until  death.  If  life  continue  for  from  ten  to  twenty  hours  the 
initial  sinking  gives  place  to  an  elevation  of  temperature.  In  fatal  cases 
the  secondary  rise  may  reach  108°  F.  or  even  higher  before  death,  but 


614  VASCULAR    DISEASES    OF    THE    BRAIX. 

in  favorable  cases  it  continues  to  oscillate  for  some  clays  between  99°  F. 
and  100.5°  F.  If  the  case  is  to  terminate  favorably  the  temperature 
now  gradually  sinks  to  the  normal,  but  if  a  fatal  termination  is  to  take 
place  the  more  or  less  stationary  temperature  of  the  first  few  days  is 
followed  by  a  rapid  and  continuous  rise,  just  as  occurs  after  the  period  of 
initial  lowering. 

Conjugate  deviation  of  the  eyes,  with  rotation  of  the  head  and  neck. 
occurs  as  a  temporary  symptom  in  all  cases  of  severe  cerebral  hemor- 
rhage, the  deviation  being  directed  away  from  the  paralyzed  side  when 
the  lesion  is  situated  in  the  hemisphere  and  towards  it  when  it  is  situated 
low  down  in  the  pons.  The  eyes  are  usually  fixed,  but  occasionally 
exhibit  slight  nystagmus.  The  rotation  may  completely  disappear  when 
the  patient  falls  asleep  and  the  symptom  usually  lasts  only  a  few  days. 

The  permanent  symptoms  of  cerebral  hemorrhage  are  the  various 
forms  of  hemiplegia  with  rigidity  of  the  paralyzed  muscles  which  will 
be  subsequently  described. 

Vaso-motor  disorders  are  generally  observed  in  the  paralyzed  limbs 
soon  after  the  attack ;  the  paralyzed  limbs  are  redder  and  warmer  than 
the  corresponding  healthy  limbs,  the  difference  in  temperature  var^nng 
from  a  fraction  of  a  degree  to  2°  F.,  and  they  may  also  become  swollen 
from  a  slight  degree  of  subcutaneous  oedema.  The  temperature  of  the 
paralyzed  limbs  gradually  decreases  and  is  eventually  lower  than  that 
of  the  sound  side,  and  when  the  oedema  disappears  the  skin  becomes 
dry  and  scal3^  Congestions  and  even  hemorrhage  of  the  lungs,  and 
extravasations  into  the  pleura,  endocardium,  mucous  membrane  of  the 
stomach,  the  suprarenal  capsules,  and  the  kidneys  frequently  accom- 
pany cerebral  hemorrhage,  and  are  often  limited  to  the  paralyzed  side 
of  the  body. 

The  trophic  disorders  consist  of  acute  bedsores,  which  may  appear  on 
the  gluteal  region  of  the  paralyzed  side  soon  after  the  attack.  Acute 
inflammation  of  one  or  more  of  the  large  joints,  or  chronic  arthritis  of 
the  small  joints,  may  begin  on  the  paralyzed  side  generally  in  from 
three  to  six  weeks  after  the  onset.  In  some  cases  the  patient  complains 
of  pain  on  pressure  in  the  paralyzed  limb,  which  is  especially  well 
marked  along  the  course  of  the  principal  nerve  trunks,  and  Cornil 
has  shown  that  it  is  most  probably  caused  by  an  inflammatory  hyper- 
trojihy  of  the  nerves  or  of  their  sheaths.  In  some  exceptional  cases 
the  paralyzed  muscles  undergo  early  and  rapid  wasting,  and  when  the 
hemiplegia  occurs  in  childhood,  the  affected  limbs  grow  more  sloAvly  than 
the  corresponding  healthy  ones,  and  the  former  are  consequently  smaller 
in  all  their  dimensions  than  the  latter.  The  skin  on  the  paralyzed  side 
sometimes  feels  thicker  than  on  the  healthy  side,  while  the  hair  some- 


IXTRACRANIAL    HEMOERHAGE.  615 

times  grows  better  on  the  affected  than  on  the  unaffected  side.  The 
nails  on  the  paralyzed  side  become  yellowish,  marked  with  ridges,  brittle, 
and  curved. 

The  mental  condition  of  the  patient  is  seldom  fully  restored.  In  most 
cases  the  intellectual  condition  is  permanently  enfeebled,  so  that  the 
patient  feels  unequal  to  any  unusual  intellectual  effort,  wdiile  in  other 
cases  the  intellect  undergoes  progressive  declension,  and  the  patient  is 
reduced  to  a  state  of  childishness  or  pronounced  dementia.  At  other 
times  the  patient  becomes  peevish,  whimsical,  irritable,  and  gives  way 
to  outbursts  of  passion.  The  disorders  of  speech  which  occur  in  cerebral 
hemorrhage  will  be  subsef{uently  described. 

2.  Meningeal  Hemorrhage. 

Etiology. — The  most  frequent  causes  of  meningeal  apoplexy  are  in- 
juries of  the  skull  producing  rupture  of  arteries,  veins,  or  sinuses, 
rupture  of  aneurisms  of  larger  arterial  branches,  and  thrombosis  of  the 
sinuses.  Meningeal  hemorrhage  may  occur  in  the  course  of  acute 
infectious  diseases,  chronic  dyscrasise,  and  progressive  paralysis  of  the 
insane,  while  the  meningeal  apoplexy  of  newborn  children  is  caused  by 
certain  accidents  attending  childbirth. 

Symptoms. — Meningeal  hemorrhage  caused  by  rupture  of  an  aneurism 
forms  the  least  complicated  form  of  the  disease,  inasmuch  as  hemor- 
rhages of  traumatic  origin  are  usually  complicated  by  other  cerebral 
symptoms.  In  severe  cases  of  uncomplicated  meningeal  hemorrhage 
the  patient  becomes  suddenly  apoplectic  without  any  warning,  or  with 
only  slight  premonitory  symptoms,  such  as  headache,  dizziness,  and 
vomiting.  The  paralysis  commonly  affects  all  four  extremities,  and 
hemiplegia  is  only  rarely  met  with.  The  onset  is  often  marked  by 
epileptiform  convulsions  and  vomiting,  profound  coma  supervenes,  and 
the  patient  dies  in  a  few  hours  or  at  most  in  a  few  days.  In  less  severe 
cases  the  patient  may  recover  consciousness  after  a  few  hours,  and  he 
then  complains  of  headache  and  is  often  delirious,  and  after  a  short  period 
of  somnolence  he  finally  becomes  comatose.  In  a  few  cases  the  symp- 
toms creep  on  gradually ;  the  patient  complains  at  first  of  headache, 
dizziness,  and  numbness  or  weakness  of  the  extremities  on  one  or  both 
sides,  and  after  a  time  he  falls  into  a  condition  of  stupor  and  ultimately 
dies  comatose. 

If  an  aneurism  of  considerable  size  has  existed  for  some  time  before 
the  occurrence  of  hemorrhage,  it  may  give  rise  to  the  symptoms  of  an 
intracranial  tumor,  which  will  be  subsequently  described. 


616  VASCULAR    DISEASES    OF    THE    BRAIX. 

In  the  meningeal  hemorrhages  of  the  newborn,  the  children  are  either 
born  dead,  or  in  a  condition  of  asphyxia,  and  often  die  soon  afterwards. 
If  respiration  is  established  the  infant  lies  in  a  comatose  condition  for 
some  days  or  weeks,  and  during  this  time  he  suffers  from  frequent  attacks 
of  convulsions,  which  are  generally  most  pronounced  on  one  side  of  the 
body.  In  such  cases  the  disease  may  prove  fatal  by  coma  or  the  patient 
may  gradually  recover  so  far  as  life  is  concerned,  but  he  remains  the 
subject  of  one  or  other  of  the  forms  of  spastic  paralysis  of  infoncy 
already  described. 

Prognosis. — The  case  will  terminate  fatally  at  an  early  period  if  the 
patient  cannot  be  roused  at  all,  and  if  the  reflex  action  of  the  conjunctiva 
is  abolished,  the  urine  and  feces  are  passed  involuntarily,  and  there  is 
well-marked  stertor,  while  the  persistence  of  even  a  slight  degree  of 
these  symptoms  without  abatement  is  a  sign  of  great  gravity.  A  (|uick, 
irregular  pulse  with  labored  respiration,  and  decided  diflSculty  of  deglu- 
tition and  articulation,  are  also  very  unfavorable  signs.  A  marked 
and  persistent  depression  of  the  pulse  is  of  fatal  significance,  while  a 
marked  and  persistent  rise  of  temperature  is  an  almost  equally  grave 
sign.  A  sudden  depression  of  temperature  with  increase  or  renewal  of 
a  preexisting  comatose  condition  is  also  of  serious  import,  indicating,  as 
it  does,  the  occurrence  of  a  fresh  hemorrhage.  Acute  bedsores  on  the 
buttock  of  the  paralyzed  side  is  a  fatal  sign. 

Treatment. — The  treatment  of  cerebral  antr'mia  must  vary  according 
as  the  disease  is  acute  or  chronic,  and  as  it  is  limited  to  the  brain  or 
affects  the  entire  body.  In  an  ordinary  faintinf/  fit  tlie  patient  should 
be  as  speedily  as  possible  placed  in  the  recumbent  posture,  and  recovery 
usually  takes  place  without  further  treatment.  If  the  symptoms  are 
more  persistent,  some  form  of  local  irritant  must  be  employed,  such  as 
sprinkling  the  face  with  cold  water,  or  flecking  it  with  the  corner  of  a 
towel  dipped  in  cold  water,  the  apj)lication  of  the  faradic  current  to  the 
surface  by  means  of  the  metallic  brush,  the  inhalation  of  ammonia  to 
stimulate  the  olfactory  and  trigeminal  nerves,  or  a  stimulating  enema. 
As  soon  as  the  patient  can  swallow,  stimulants,  such  as  coffee  or  brandy, 
must  be  given,  especially  if  the  heart's  action  be  feeble.  In  severe 
cases  of  cerebral  ansemia,  after  profuse  hemorrhage,  the  body  of  the 
patient  ought  to  be  covered  with  warm  clothing  and  surrounded  by 
bottles  containing  hot  water,  and  in  order  to  increase  the  flow  of  blood 
towards  the  brain  the  head  ought  to  be  kept  in  a  low  position,  while 
pressure  is  maintained  over  the  abdominal  and  axillary  arteries.  In 
cases  of  severe  and  prolonged  anaemia  from  loss  of  blood  transfusion 
ought  to  be  tried  as  a  last  resort.  The  cerebral  anaemia  which  arises 
during  the  course  of  acute  diseases  must  be  treated  by  the  judicious  use 


INTKACEANIAL    HEMOERHAGE.  617 

of  wine  and  nourishing  diet,  and  if  the  ease  admit  of  it  by  such  tonics 
as  quinine,  iron,  and  arsenic.  When  delirium  or  other  form  of  cerebral 
excitement  accompanies  the  aniBniia,  the  great  aim  of  treatment  should 
be  to  procure  sleep,  and  a  full  dose  of  chloral  or  better  still  an  opiate 
should  be  administered.  Hydrocephaloid  disease  should  be  treated  on 
the  same  general  principles  as  other  forms  of  cerebral  anaemia  and  in 
addition  the  diarrhoea  or  other  disease  which  has  caused  the  ant^mia 
must  be  attended  to. 

Occlusion  of  cerebral  vessels  must  be  treated  on  the  same  general 
principles  as  hemorrhage  from  them,  but  in  embolus  the  cardiac  compli- 
cation must  be  subjected  to  treatment,  while  in  thrombosis  the  presence 
either  of  syphilitic  endarteritis  or  of  atheromatous  degeneration  of  the 
arteries  must  be  borne  in  mind  and  the  appropriate  treatment  adopted 
for  each. 

Congestion  of  the  brain  must  be  treated  by  rest  in  the  recumbent 
position  with  the  head  raised,  ice  to  the  head,  and  active  purgation. 
The  diet  should  be  plain  and  unstimulating,  but  nourishing.  Moderate 
doses  of  ergot  are  supposed  to  have  a  favorable  influence  on  the  disease. 

In  cerebral  hemorrhage  the  aims  of  treatment  are  (1)  to  avert  a 
threatened  attack  ;  (2)  to  treat  the  apoplectic  condition ;  (3)  to  allay 
excitement  during  the  inflammatory  reaction  ;  and  (4)  to  improve  the 
permanent  symptoms. 

(1)  Prophylactic  Treatment. — When  a  person  complains  of  any  of 
the  usual  premonitory  symptoms  of  apoplexy  the  treatment  must  vary 
according  to  the  state  of  the  general  health.  The  condition  of  the  heart 
and  bloodvessels  must  be  carefully  explored,  and  the  urine  must  be 
tested  for  albumen  and  sugar,  and  the  treatment  must  be  adapted  to  meet 
any  disorder  of  the  general  health  which  may  be  discovered.  Saline 
purgatives  are  generally  useful  by  lowering  the  arterial  tension,  and 
during  the  continuance  of  threatening  symptoms  the  patient  should  be 
kept  quiet  in  a  darkened  room  and  cold  applied  to  the  head. 

(2)  The  apoplectic  attack  must  be  treated  by  absolute  rest,  and  cold 
to  the  head,  and  if  the  arterial  tension  be  high  a  moderate  bleeding  may 
do  good,  but  the  severe  general  bleeding  practised  a  few  years  ago  is 
quite  inadmissible.  When  there  are  signs  of  cardiac  failure,  or  when 
the  breathing  is  intermittent  or  assumes  the  Cheyne-Stokes  character, 
then  a  stimulating  treatment  must  be  adopted,  but  the  common  practice 
of  applying  blisters  to  the  shorn  scalp  or  to  the  nape  of  the  neck,  or 
mustard  plasters  to  the  calves  of  the  legs,  is  useless  and  ought  to  be 
strongly  condemned. 

If  the  attack  is  preceded  or  accompanied  by  recurring  epileptiform 
attacks,  or  if  the  patient  is  restless  and  there  is  more  or  less  of  delirious 


618  VASCULAR    DISEASES    OF.    THE    BRAIX. 

Avandering,  bromide  of  potassium  nia}^  be  given.  If  the.  bowels  are 
constipated  an  enema  containing  castor  oil  or  oil  of  turpentine  should 
be  administered,  or  two  drops  of  croton  oil  may  be  given  in  a  suitable 
vehicle  or  placed  on  the  back  of  the  tongue.  The  state  of  the  bladder 
should  be  carefully  examined  and  a  catheter  used  if  necessary. 

(3)  If  the  patient  survive  the  first  shock  of  the  apoplectic  attack, 
the  less  we  interfere  during  the  first  days  the  better.  He  must  be  kept 
as  quiet  as  possible  both  in  body  and  mind,  his  diet  should  consist 
of  liquid  nourishment,  and  the  state  of  his  secretions  and  excretions 
should  be  carefully  regulated.  Cold  should  be  applied  when  the  symp- 
toms of  inflammatory  reaction  appear,  and  if  the  patient  complain  of 
headache,  or  there  be  persistent  wakefulness  or  delirium,  a  full  dose  of 
bromide  of  potassium,  or  even  an  opiate  or  chloral  should  be  given. 
During  this  period  great  care  must  be  taken  to  prevent  bedsores  on  the 
paralyzed  side  by  paying  constant  attention  to  the  state  of  the  bedding 
and  securing  extreme  cleanliness.  In  severe  cases  the  patient  should, 
when  practicable,  be  placed  from  the  first  on  a  water  bed. 

(4)  The  most  effectual  method  of  promoting  the  improvement  of  the 
paralyzed  nerves  and  muscles  is  a  thorough  attention  to  the  general 
health  of  the  patient,  and  tlie  treatment  pro})er  for  each  case  will  depend 
upon  his  age,  habits,  and  constitution,  and  on  the  presence  or  absence 
of  any  concomitant  disease.  The  general  principles  of  treatment 
are  to  take  care  that  the  patient  has  a  sufficiency  of  easily  digestible 
and  nutritious  food ;  tliat  all  circumstances  which  might  cause  mental 
excitement  are  avoided ;  and  that  he  has  a  due  amount  of  repose  and 
sleep.  In  the  hemiplegias  of  elderly  people,  in  which  miliary  aneu- 
risms may  be  presumed  to  exist,  care  must  be  taken  that  the  circulation 
is  not  subjected  to  any  sudden  strain,  and  it  is,  therefore,  necessary  to 
keep  the  bowels  moderately  open  lest  straining  at  stool  should  induce 
another  attack.  The  patient  should  take  open  air  exercise  by  walking 
on  level  ground,  or  in  a  chair  or  carriage,  and  much  good  may  be  done 
by  sponging  with  salt  water.  When  there  is  advanced  arterial  degenera- 
tion or  high  arterial  tension  the  water  ought  to  be  tepid,  and  heniiplegic 
patients,  as  a  rule,  should  only  use  baths  of  moderate  temperature. 
Iodide  of  potassium  is  the  most  likely  drug  to  promote  the  absorption 
of  the  clot,  and  its  administration  may  be  commenced  immediately  after 
the  febrile  symptoms  of  the  inflammatory  reaction  have  subsided.  In 
ordinary  cases,  from  three  to  five  grain  doses  three  times  a  day  will 
suffice ;  but  if  the  hemorrhage  is  caused  by  premature  degeneration  of 
the  arteries  from  syphilis,  it  Avill  be  advisable  to  give  from  fifteen  to 
twenty  grain  doses  three  times  a  day,  and  in  some  cases  it  will  be  neces- 
sary to  give  mercury  in  some  form  along  with  the  iodine  salt. 


INTHACRANTAL    HEMORRHAGE.  619 

The  local  treatment  of  the  paralyzed  limbs  consists  of  passive  move- 
ments, and  friction  of  the  skin  by  means  of  a  flesh  brush,  flannel,  or 
the  palm  of  the  hand.  After  a  time  the  patient  should  be  directed  to 
move  the  paralyzed  limbs  by  voluntary  effort,  and  various  gymnastic 
exercises  may  be  adopted  to  bring  the  paralyzed  muscles  into  separate 
and  combined  action.  The  constant  current  may  be  employed  by 
placing  one  electrode  on  each  mastoid  process,  or  one  on  a  mastoid 
process  and  the  other  on  the  nape  of  the  neck,  but  in  this  method  only 
feeble  currents  should  be  used,  and  the  duration  of  the  application 
should  not  exceed  three  minutes.  According  to  another  method,  the 
current  is  passed  through  the  paralyzed  nerves  and  muscles  in  the 
usual  way.  The  faradic  current  has  been  employed  in  contractures 
for  the  purpose  of  acting,  not  on  the  contracted  muscles,  but  upon  their 
antagonists,  but  this  method  has  not  been  productive  of  much  good. 
The  methods  used  to  promote  the  recovery  of  the  paralyzed  muscles 
are  also  the  best  remedies  for  the  sensory  disorders  which  are  often 
present  in  cases  of  hemiplegia. 


CHArXER    XYT. 
ENCEPHALITIS. 

Etiology. — The  most  freciuent  cause  of  acute  inflammatiou  aud 
abscess  of  the  brain  is  recent  injury.  When  air  gains  access  to  the 
interior  of  the  skull  through  an  open  wound,  encephalitis  becomes  com- 
plicated with  meningitis,  but  contusion  of  the  brain  may  give  rise  to  it 
in  the  absence  of  any  perforating  wound.  Encephalitis  may  be  set  up 
by  diseases  of  the  bones  of  the  skull,  such  as  caries,  or  inflammatory 
action  may  be  transmitted  to  the  brain  from  diseases  of  the  nose, 
antrum  of  Highmore,  and  orbit,  while  abscess  of  the  brain  frequently 
results  from  disease  of  the  middle  or  internal  ear.  Multiple  cerebral 
abscesses  occur  in  connection  with  acute  febrile  affections,  such  as 
typhoid  and  scarlet  fevers,  and  in  putrid  bronchitis  and  bronchiectasis, 
ulcerative  endocarditis,  and  other  pytrmic  affections.  Focal  diseases  of 
the  brain  like  tumors,  hemorrhage,  thrombosis,  and  embolism,  often  set 
up  surrounding  inflammation  in  the  brain,  and  in  some  cases  enceph- 
alitis may  be  of  idiojjathic  origin. 

DIFFUSED  OK  GENERAL  ENCEPHALITIS. 

Cases  of  uncomplicated  general  encephalitis  are  not  very  common, 
most  of  the  cases  Avhich  have  l)een  reported  as  examples  of  this  disease 
being  examples  of  cerebral  meningitis,  or,  more  strictly  speaking,  of 
meningo-encephalitis.  The  symptoms  of  simple  encephalitis  are  pyrexia, 
a  busy  and  talkative  but  not  violent  delirium,  passing  on  to  somnolence 
and  finally  to  coma.  The  presence  of  spasms  Avould  seem  to  indicate 
a  complication  with  meningitis,  while  the  appearance  of  partial  or  com- 
plete hemiplegia  Avould  shoAv  that  the  disease  is  more  pronounced  on  one 
side  than  on  the  other,  and  therefore  that  the  inflammation  is  partial. 

PARTIAL  OR  LOCAL  ENCEPHALITIS. 

Local  encephalitis  may  occur  as  1,  an  idiopathic  affection  in  children, 
when  it  has  been  named  poUencephalitis  acuta  infantium;  2,  as  the 
result  of  an   injury;  3,  as  a   consequence  of  pyaemic  infection;  and 


PARTIAL    OR    LOCAL    E  XC  E  P  H  ALl  TIS  .  621 

4,  as  a  secondary  result  of  a  focal  disease  like  (a)  abscess,  [b)  hemor- 
rhage, (c)  softening  from  occlusion  of  vessel,  and  [d)  tumor. 


1.    POLIEXCEPHALITIS    AcUTA    InFANTIUM. 

Acute  inflammation  of  the  brain  occurs  in  infancy  between  the  ages 
of  one  and  six  years.  The  attack  may  follow  measles  or  scarlet  fever, 
or  be  set  up  by  a  blow  on  the  head,  but  in  the  majority  of  cases  no 
exciting  cause  can  be  assigned,  and  the  subjects  of  the  disease  do  not 
even  seem  to  belong  to  neuropathic  families.  The  attack  begins  sud- 
denly with  fever,  vomiting,  and  convulsions,  and  the  child  falls  into  an 
apoplectic  condition  which  may  last  two  or  three  days,  occasionally 
one  or  two  weeks,  or  even  longer.  The  spasms  are  generally  more 
pronounced  on  one  side  of  the  body  than  on  the  other,  and  are  often 
strictly  unilateral ;  after  a  longer  or  shorter  time  the  convulsed  limbs 
become  more  or  less  completely  paralyzed.  It  is  possible  that  many 
of  these  cases  are  fatal,  but  in  other  cases  the  child  gradually  re- 
covers, except  that  he  is  the  subject  of  a  permanent  hemiplegia.  The 
further  progress  of  this  aff'ection  has  been  already  described  under  the 
name  of  spasmodic  hemiplegia  of  infancy,  of  Avhich  unilateral  atrophy 
of  the  brain  is  the  anatomical  counterpart. 


2.  Traumatic  Local  Encephalitis. 

When  a  contusion  in  the  interior  of  the  brain  has  taken  place,  the 
patient  first  suffers  from  the  usual  symptoms  of  concussion,  and  it  is 
only  when  these  have  disappeared  that  the  usual  symptoms  of  a  local 
encephalitis  can  be  recognized.  The  patient  lies  in  a  semiconscious 
condition,  and  when  roused  complains  of  headache  and  dizziness,  and 
staggers  on  attempting  to  walk.  The  pupils  are  variable  in  size,  but 
they  are  generally  equal  and  react  slowly  to  light.  The  countenance 
is  usually  suffused,  but  at  times  it  turns  pale,  and  the  pulse,  which  was 
frequent  and  irregular  during  the  stage  of  concussion,  sinks  to  sixty  or 
seventy  beats,  but  the  thermometer  may  indicate  the  existence  of  fever 
of  remittent  type.  When  the  encephalitis  is  situated  in  the  frontal, 
temporal,  or  occipital  lobes,  the  symptoms  may  be  so  slight  that  the 
patient  feels  quite  well  in  a  few  days,  or  suffers  for  a  week  or  two  from 
very  indefinite  symptoms.  Suddenly,  however,  more  pronounced  symp- 
toms become  manifest;  the  fever,  which  still  continues  of  irregular 
type,  becomes  more  intense;  dizziness  and  headache  become  more 
marked ;  vomiting  is  not  infrequently  present :  the  pupils  are  dilated 


622  ENCEPHALITIS. 

and  fixed ;  the  pulse  is  slow ;  and  the  patient  fells  into  a  condition  of 
stupor,  which  may  be  accompanied  by  delirium,  or  may  pass  directly 
into  complete  unconsciousness. 

As  the  case  progresses  the  symptoms  of  a  localized  disease  may 
appear,  consisting  at  first  of  spasmodic  phenomena,  such  as  rolling  of 
the  eyes,  twitchings  of  the  face  or  hands,  or  more  decided  clonic  con- 
vulsions of  the  limbs,  or  even  a  general  convulsion,  but  these  are  soon 
followed  by  paralysis  of  the  abducens,  motor  oculi,  or  facial  nerve,  and 
in  a  few  cases  by  hemiparesis  or  hemiplegia.  The  stupor  now  grows 
deeper,  the  urine  and  feces  are  passed  involuntarily,  the  previously  slow 
pulse  becomes  quick  and  irregular,  and  death  takes  place  in  coma. 
The  course  of  the  temperature  is  variable,  but  a  continuous  elevation 
until  death  is  exceptional. 

The  duration  of  local  encephalitis  varies  greatly,  and  an  abscess  of 
the  brain  has  occasionally  been  found  as  early  as  the  fifth  day  after  the 
injury,  and  when  air  gains  access  to  the  brain  through  an  open  wound, 
and  suppuration  occurs,  the  disease  may  terminate  fatally  at  a  much 
earlier  period.  The  patient  may  occasionally  be  restored  to  compara- 
tive health  after  an  attack  of  traumatic  encephalitis.  The  inflamma- 
tory focus  may  be  transformed  into  a  relatively  innocuous  condition, 
but  even  in  those  favorable  cases  chronic  changes  of  a  diffused  character 
are  occasioned  which  give  rise  to  more  or  less  permanent  symptoms. 
The  symptoms  consist  generally  of  some  form  of  mental  deterioration, 
such  as  melancholia,  chronic  mania,  or  a  condition  resembling  general 
paralysis.  Injuries  of  the  skull  are  often  followed  by  epilepsy,  and 
may  be  the  starting-point  of  intracranial  growths,  while  a  fall  on  the 
back  of  the  head  sometimes  gives  rise  to  diabetes. 

3.  Acute  Py.emic  Encephalitis. 

Acute  pycemic  encephalitis  is  frequently  ushered  in  by  rigors,  but 
these  being  symptomatic  of  the  general  disease,  do  not  indicate  the 
approaching  complication.  The  first  signs  of  the  brain  affection  are 
afforded  by  severe  headache,  which  is  usually  frontal;  dizziness;  deli- 
rium or  somnolence ;  unilateral  convulsions ;  and  formication  or  numb- 
ness of  the  extremities.  The  disease  makes  rapid  progress  and  the 
headache  now  becomes  intense,  the  dizziness  is  so  gi*eat  that  the  patient 
is  unable  to  sit  up  in  bed,  the  mind  is  confused,  and  the  delirium  or 
somnolent  condition  of  the  first  stage  soon  gives  place  to  profound 
coma,  which  proves  rapidly  fatal.  The  intensity  of  the  febrile  symp- 
toms is  variable,  but  in  many  cases  there  is  a  considerable  elevation  of 
temperature. 


partial  or  local  e  xcep ii alitis.  623 

4.  Encephalitis  Complicating  Pre-existing  Lesions  of  the 

Brain. 

a.  Acute  Abscess  2cnth  Encephalitis. 

The  symptoms  caused  by  the  acute  encephalitis  which  accompanies 
caries  of  the  petrous  bone  are  often  obscured  by  coexisting  meningitis 
and  thrombosis  of  the  lateral  sinuses.  An  abscess  in  the  temporal 
lobe  may  attain  a  considerable  size,  and  cause  general  symptoms  of 
compression  before  giving  rise  to  symptoms  of  local  disease,  inasmuch 
as  this  lobe  does  not  contain  any  direct  sensory  or  motor  conducting 
tracts.  Acute  abscesses  of  the  temporal  lobe  are  consequently  seldom 
recognized  during  life.  The  symptoms  of  acute  abscess,  from  otorrhoea, 
or  from  caries  of  the  other  bones  of  the  skull,  begin  with  severe  headache, 
vomiting,  ringing  in  the  ears,  confusion  of  ideas,  loss  of  memory,  and 
delirium.  As  the  disease  advances  the  headache  becomes  more  and  more 
intense,  the  delirium  gives  place  to  stupor,  epileptiform  convulsions 
supervene,  and  the  case  soon  terminates  fatally  amidst  profound  coma. 
Fever  of  variable  type  is  usually  present,  the  pulse  is  slow,  and  the 
pupils  are  contracted  and  sluggish.  In  some  cases  of  abscess  of  the 
temporal  lobe  the  general  symptoms  are  complicated  by  those  of  a 
localized  disease,  and  in  these  cases  the  abscess,  which  has  rapidly 
attained  to  a  considerable  size,  compresses  the  fibres  of  the  internal 
capsule  or  the  cerebral  peduncle,  and  thus  causes  an  incomplete  hemi- 
plegia with  various  sensory  disorders,  as  well  as  paralysis  of  the  oculo- 
motor nerve,  and  occasionally  of  the  facial.  A  few  cases  are  associated 
with  acute  meningitis  or  thrombosis  of  the  lateral  sinus. 

h.  Chronic  Abscess  with  Encephalitis. 

Chronic  abscess  of  the  brain  may  be  divided  into  {a)  primary,  and 
(b)  secondary  chronic  abscess. 

{a)  Primary  Chronic  Abscess. 

Primary  chronic  abscess  is  usually  caused  by  some  injury  of  the 
brain.  All  the  symptoms,  or  nearly  all,  may  disappear  soon  after  the 
injury,  and  a  period  relatively  free  from  symptoms  may  follow,  forming 
the  latent  stage  of  chronic  abscess.  The  average  duration  of  the  latent 
stage  is,  according  to  Lebert,  from  one  to  two  months,  but  the  period 
may  vary  in  individual  cases  from  a  few  days  to  years.  When  once  a 
chronic  abscess  is  formed,  the  symptoms  caused  by  it  are  more  or  less 


624  ENCEPHALITIS. 

similar  to  those  of  cere1)ral  tumor,  and  when  the  former  is  situated  in 
the  motor  areas  of  the  cortex  and  centrum  ovale,  or  injure  the  sensory 
peduncular  fibres,  the  symptoms  of  a  local  lesion  are  present  from  the 
beo-innintr.  The  symptoms  may  be  divided  into  those  of  (1)  the  latent, 
and  (2)  the  tei'minal  stages. 

(1)  Sy7nptoms  of  ihe  Latent  Period. 

The  symptoms  of  the  latent  stage  are  those  of  a  moderate  degree  of 
intracranial  pressure.  These  consist  of  constant  headache  with  parox- 
ysmal exacerbations,  and  slight  febrile  disturbance,  dizziness,  nausea, 
and  occasionally  vomiting.  The  headache  may  be  limited  to  the  spot 
where  the  injury  was  received,  or  correspond  to  the  part  of  the  brain 
where  the  abscess  is  situated,  the  latter  being  often  at  a  point  of  the 
brain  exactly  opposite  the  seat  of  injury.  l*aroxysmal  exacerbations 
of  the  headache  are  indicative  of  congestion  around  the  abscess,  and 
when  these  frequently  recur  the  abscess  is  likely  to  prove  fiital  within  a 
l)rief  space  of  time.  In  some  cases  monospasms,  monoplegia,  or  other 
indications  of  a  local  disease  in  the  brain  are  superadded  to  the  general 
symptoms  just  described. 

In  other  cases  the  patient  has  intervals  of  comparative  freedom  from 
all  cerebral  symptoms,  but  in  the  midst  of  comparative  health  he  may 
suddenly  complain  of  intense  headache,  and  soon  fall  into  a  deep  but 
transitory  coma  of  several  hours"  duration,  from  which  he  rapidly  re- 
covers, such  attacks  being  probably  due  to  sudden  pressure  on  the 
brain  from  congestion. 

("2)  Symptoms  of  the  Terminal  Period. 

When  once  the  terminal  period  begins,  abscess  of  the  ])rain  generally 
leads  to  death  in  a  few  days.  The  symptoms  of  this  period  differ  widely 
in  individual  cases,  and  the  following  groups  may  be  distinguished  : 

(a)  TerniinaJ  oedema  of  the  brain  is  the  most  usual  mode  of  termina- 
tion of  chronic  abscess.  In  the  majority  of  cases  the  tissues  of  the 
brain  are  compressed  to  such  an  extent  that  death  by  coma  results  in 
two  or  three  days,  while  in  a  few  cases  the  course  of  the  symptoms  is 
characterized  by  temporary  improvements  and  aggravations,  so  that  the 
fatal  issue  may  be  delayed  for  some  time.  In  some  cases  there  may  be 
a  transitory  initial  stage  of  irritation,  characterized  by  mental  irritability, 
restlessness,  illusions,  violent  delirium,  and  a  slight  elevation  of  temper- 
ature. The  irritative  symptoms  soon  give  place  to  those  of  depression, 
the  patient  complains  of  headache,  the  temperature  falls,  the  pulse  is 
slow,  the  pupils  are  dilated  and   react  feeblv  to  light,  there  is  mental 


i 


PAKTIAL    OR    LOCAL    ENCEPHALITIS.  625 

confusion,  and  the  patient  falls  into  a  somnolent  condition,  from  Avhich 
he  may  be  roused  temporarily  when  pressed  by  questions ;  but  in  a 
short  time  coma  supervenes,  and  the  case  soon  terminates  fatally,  the 
pulse  becoming  small,  quick,  and  irregular  before  death. 

The  symptoms  of  local  disease  which  may  have  been  present  during 
the  latent  stage  of  the  abscess  are  variously  modified  in  the  terminal 
stage.  Partial  convulsions,  which  may  have  been  present,  become  more 
violent  and  are  soon  followed  by  paralysis,  or  they  may  become  trans- 
formed into  a  series  of  epileptiform  attacks  terminating  in  coma. 
General  convulsions  are  sometimes  caused  by  abscess  situated  in  the 
latent  regions  of  the  hemisphere,  and  these  are  usually  followed  by  pro- 
found coma. 

(b)  Rupture  of  the  Abscess  on  the  Surface  of  the  Brain. — When 
abscesses  make  their  way  to  the  surface  of  the  brain,  an  acute  and 
rapidly  fatal  meningitis  generally  results.  The  symptoms  of  irritation 
are  at  first  predominant,  but  the  patient  soon  becomes  unconscious,  and 
dies  comatose  in  a  short  time. 

(c)  Perforation  of  the  Abscess  into  the  Ventricle. — This  occurrence 
causes  a  group  of  symptoms  which  may  be  recognized,  if  the  existence 
of  an  abscess  have  been  previously  suspected.  A  sudden  cerebral 
attack,  attended  by  bilateral,  but  more  or  less  partial  convulsions,  such 
as  spasms  of  both  legs,  or  of  the  facial  muscles  on  both  sides,  is  an 
indication  of  rupture  into  the  ventricles,  provided  the  patient  be  not 
already  in  an  unconscious  condition.  General  convulsions  have  some- 
times been  observed.  Clonic  spasms  of  the  ocular  muscles  soon  appear, 
caused  probably  by  irritation  of  the  corpora  quadrigemina.  The  patient 
becomes  rapidly  unconscious,  hemiplegia  and  death  in  profound  coma 
take  place  generally  in  from  four  to  twenty-four  hours  after  the  rupture 
of  the  abscess. 

(d)  Abscess  of  the  cerebellum  may  terminate  suddenly  from  arrest  of 
the  respiratory  functions  produced  by  pressure  on  the  medulla  oblongata. 

(e)  Occasionally  the  brain  is  found  in  a  condition  of  remarkable 
antemia,  and  in  such  cases  the  immediate  cause  of  death  is  not  evident. 

(b)  Secondary  Chronic  Abscess  of  the  Brain. 

Secondary  chronic  abscesses  are  generally  caused  by  affections  of 
the  inner  ear.  The  diagnosis  of  the  presence  of  chronic  abscess  of  the 
brain  is  difficult,  inasmuch  as  only  a  small  proportion  of  such  cases  give 
rise  to  characteristic  symptoms.  When  the  abscess  is  encapsulated  it 
may  remain  latent  for  a  long  time,  so  that  no  disease  of  the  brain  is 
suspected  until  the  terminal  period.  Even  the  terminal  symptoms  pre- 
sent varieties   which   tend   to  obscure  the  diagnosis,   these  symptoms 

40 


626  ENCEPHALITIS. 

sometimes  resembling  those  of  diffuse  meningitis,  and  at  other  times 
those  of  thrombosis  of  a  sinus. 

Varieties. — The  following  varieties  of  chronic  abscess  secondary  to 
disease  of  the  ear  may  be  distinguished :  (1)  Chronic  abscess  with 
distinct  typical  course ;  (2)  Chronic  abscess  Avith  terminal  stage  alone 
distinct ;  (3)  Chronic  abscess  with  thrombosis  of  the  lateral  sinus  ;  (4) 
Chronic  abscess  complicated  during  the  terminal  period  by  meningitis. 

(1)  In  affections  of  the  inner  ear  abscess  may  form  in  the  temporo- 
sphenoidal  lobe.  In  a  long-standing  case  of  disease  of  the  internal  ear, 
where  ric^ors  and  other  general  inflammatory  symptoms  are  associated 
with  severe  pain  in  the  head,  vomiting,  convulsions,  and  other  cerebral 
symptoms,  the  formation  of  an  abscess  in  the  brain  may  be  suspected. 
These  symptoms  may  pass  off,  and  the  patient  enjoy  apparent  health 
for  months,  with  probably  occasional  headaches.  The  terminal  stage  is 
announced  by  intense  headache  and  dizziness  soon  followed  by  loss  of 
consciousness  and  stertorous  breathing.  Consciousness  may  be  partially 
restored  in  a  few  hours,  and  the  patient  then  suffers  from  intense  head- 
ache and  vomiting.  After  a  short  time  the  patient  lapses  a  second  time 
into  a  semiconscious  condition,  and  convulsions,  generally  unilateral, 
supervene.  Spasm  followed  by  paralysis  of  the  ocular  muscles  is  not 
an  unfrequent  symptom,  and  when  the  abscess  is  so  large  that  it  extends 
to  the  lenticular  nucleus  and  compresses  the  internal  capsule,  or  the 
fibres  of  the  pyramidal  tract  in  the  crusta,  a  certain  degree  of  hemi- 
plegia may  be  present. 

(2)  Chronic  abscess  of  the  brain  is  sometimes  observed  in  cases  of 
caries  of  the  petrous  bone,  in  which  the  terminal  symptoms  have  not 
been  preceded  by  those  indicative  of  irritation  or  encephalitis. 

(3)  Chronic  abscess  of  the  brain  sometimes  precedes,  at  other  times 
succeeds  to  thrombosis  of  the  lateral  sinus.  The  chief  initial  symp- 
toms are,  besides  those  of  the  ear  affection,  dizziness,  intense  headache, 
and  occasionally  transitory  delirium,  followed  by  somnolence.  The 
patient  suffers  from  frequently  repeated  rigors  if  the  temperature  of  the 
body  be  raised,  and  the  fever  assumes  a  remittent  type.  In  the  further 
progress  of  the  case  the  symptoms  may  pursue  either  of  two  directions. 
The  symptoms  may  be  those  of  progressively  increasing  pressure  upon 
the  brain,  ending  in  coma,  or  the  general  symptoms  indicative  of  com- 
pression may  be  associated  with  those  of  localized  disease,  provided  the 
abscess  has  attained  a  sufficient  size  to  press  upon  the  internal  capsule. 
General  convulsions  may  occur  immediately  before  death. 

(4)  Chronic  abscess  of  the  brain  may  be  complicated  during  the 
terminal  period  by  meningitis,  and  when  the  initial  stage  of  the  former 
is  latent,  the  terminal  symptoms  may  be  so  similar  to  those  of  primary 


PARTIAL    OR    LOCAL    ENCEPHALITIS.  627 

acute  meningitis  that  the  two  aiFections  cannot  be  distinguished  from 
one  another  during  life. 

e.  Encephalitis  Secondary  to  Hemorrhage. 

The  patient  may  have  made  a  good  recovery  from  the  early  symptoms 
of  an  apoplectic  attack,  but  several  days  afterwards  there  is  a  secondary 
elevation  of  temperature,  and  the  pulse  becomes  hard  and  frequent. 
The  patient  complains  of  headache,  or  he  may  suflFer  from  slight  wander- 
ing and  confusion  of  ideas  or  fall  into  a  somnolent  condition.  The 
general  are  soon  followed  by  local  symptoms,  consisting  usually  of  the 
well-known  secondary  contractures.  Some  patients  may  manifest  only 
a  slight  tremor  of  the  paralyzed  limbs ;  in  others  the  flexors  are  in  a 
state  of  contracture ;  and  in  a  third  series  of  cases  these  conditions 
alternate.  The  temperature  of  the  paralyzed  side  is  often  considerably 
elevated,  and  anomalies  in  the  secretion  of  sweat  are  observed.  The 
somnolence  may  now  increase  to  a  deep  sopor  which  lasts  several  days, 
and  may  pass  into  a  profound  or  fatal  coma.  In  cases  that  recover 
symptoms  frequently  persist  Avhich  show  that  a  chronic  encephalitis  is 
established.  The  patient  suffers  from  persistent  headache,  and  frequent 
attacks  of  dizziness,  while  he  is  subject  to  congestive  attacks  each  of 
which  may  cause  new  convulsions  in  the  paralyzed  limbs.  The  para- 
lyzed limbs  are  generally  subject  to  pains  of  variable  character,  which 
may  be  situated  in  the  joints,  bones,  skin,  or  muscles.  Secondary  en- 
cephalitis is  also  the  chief  cause  of  the  atrophy  of  the  brain  found  in 
many  of  these  patients  and  which  is  always  associated  with  profound 
psychical  disturbances. 

d.  Encephalitis  Secondary  to  Thrombosis  and  Embolism. 

After  the  formation  of  softening  from  occlusion  of  a  vessel  in  the 
brain,  a  febrile  condition,  attended  by  a  drowsy  delirium  or  somnolence, 
often  continues  for  some  time,  and  either  develops  into  permanent 
imbecility,  or  gives  place  to  partial  restoration  of  the  mental  faculties. 
When  partial  recovery  takes  place  the  patient  is  affected  with  weak- 
ness of  memory,  irregular  and  causeless  outbursts  of  temper,  and  a 
disposition  to  shed  tears  or  to  laugh  without  adequate  cause.  The 
patient  is  liable  to  congestive  attacks  which  cause  temporary  uncon- 
sciousness, and  during  these  new  foci  of  softening  may  be  developed  in 
the  brain. 

In  senile  encephalomalacia  the  symptoms  of  secondary  encephalitis 
are  caused  by  an  increase  of  the  intracranial  pressure  on  the  one  hand 
and  irritation  of  the  surrounding  parts  on  the  other.  The  symptoms 
of  inflammatory  reaction  are  slight,  and  when  a  certain  degree  of  senile 


628  ENCEPHALITIS. 

atrophy  of  the  brain  had  existed  previous  to  the  occurrence  of  the  attack, 
the  mental  fimctions  become  progressively  abolished  without  being  pre- 
ceded by  symptoms  of  active  irritation  or  by  those  which  indicate  a 
gradual  compression  of  the  brain. 

e.  Encephalitis  Secondary  to  Tumor. 

The  symptoms  which  may,  with  probability,  be  ascribed  to  encephalitis 
durino-  the  growth  of  a  cerebral  tumor,  are  the  occurrence  of  sudden 
apoplectiform  attacks,  the  rapid  conversion  of  slight  muscular  weakness 
into  complete  paralysis,  partial  convulsions  followed  by  paralysis,  general 
convulsions,  the  sudden  appearance  of  sensory  disorders  in  the  para- 
lyzed or  partially  paralyzed  limbs,  and  the  gradual  development  of  coma. 
When,  however,  coma  is  suddenly  developed  it  is  more  likely  to  be 
caused  by  hemorrhage  or  sudden  oedema  than  by  ence])halitis.  Every 
attack  of  encephalitis  is  attended  by  violent  headache,  but  the  symptom 
may  be  caused  by  a  congestive  swelling  of  the  tumor  itself. 

Morbid  Anatomy. — In  encephalitis  the  affected  tissue  assumes  a 
reddish  color,  and  is  studded  with  a  num1)er  of  capillary  extravasations, 
which  are  followed  by  more  or  less  oedema.  The  affected  portion  of  the 
brain  becomes  voluminous  and  the  cut  surface  rises  above  the  level  of 
the  surrounding  tissues.  An  encephalitis  of  slight  intensity  and  small 
extent  may  undergo  complete  repair.  At  other  times  the  focus  under- 
goes destructive  changes  and  its  contents  become  converted  into  a  thick 
emulsion,  colored  brownish  or  yellowish  by  blood  pigment.  After  a 
time  a  focus  of  yellow  softening  forms  which  gradually  becomes  more 
colorless,  and  at  last  may  be  transformed  into  a  cavity  which  is  filled 
Avith  a  thin  milky  fluid.  Later,  the  focus  manifests  a  delicate  stroma 
consisting  of  connective  tissue  supplied  with  fine  bloodvessels,  and 
the  interspaces  of  which  are  filled  by  a  thin  turbid  fluid.  In  other 
cases  a  local  encephalitis  leads  to  the  production  of  a  firm  sclerotic 
cicatrix.  These  cicatrices  are  situated  usually  near  the  surface  of  the 
brain  and  only  rarely  in  its  interior ;  they  are  of  a  dirty  white  color, 
tough  and  firm,  and  the  tissue  surrounding  them  becomes  atrophied  so 
that  the  affected  hemisphere  is  less  th;in  the  other.  In  a  large  number 
of  cases  the  encephalitic  focus  is  transformed  into  a  collection  of  pus, 
forming  either  an  acute  or  chronic  abscess.  An  acute  abscess  has  a 
tendency  to  spread  in  every  direction,  and  presents  an  irregular  cavity 
in  the  substance  of  the  brain,  the  walls  of  which  have  a  rough  and 
shaggy  surface.  As  the  pus  in  the  central  cavity  accumulates,  so  much 
pressure  is  exerted  on  the  surrounding  tissue  that  the  circulation  is 
arrested  and  this  leads  to  further  destruction  and  to  advance  of  the 
abscess.     Chronic  abscesses  of  the  brain  possess  a  fibrous  capsule  which 


PARTIAL    OR    LOCAL    ENCEPHALITIS.  629 

may  attain  to  a  thickness  of  several  millimetres.  The  internal  surface 
of  the  limiting  membrane  is  smooth,  and  has  an  opaque  yellowish-white 
appearance  owing  to  a  continuous  layer  of  cells  Avhich  are  in  a  state  of 
fatty  degeneration.  The  pus  of  the  abscess  is  of  a  greenish  color,  greasy 
consistence,  odorless,  and  gives  an  acid  reaction.  After  a  time  the 
abscess  enlarges  so  as  to  raise  considerably  the  general  intracranial 
pressure,  and  extensive  yellow  softening  may  occur  in  the  surrounding 
tissues  from  arrest  of  their  nutrition.  Both  acute  and  chronic  abscesses 
may  give  rise  to  perforations  on  the  surface  of  the  brain  and  into  the 
ventricles,  extensive  oedema  or  anaemia  of  the  brain  from  increase  of 
the  intracranial  pressure,  and  chronic  internal  hydrocephalus  when  the 
abscess  is  situated  in  the  cerebellum  in  such  a  position  that  it  lessens 
the  cavity  of  the  fourth  ventricle  or  of  the  Sylvian  aqueduct. 

Morbid  Physiology. — Acute  encephalitis  gives  rise  to  general  symp- 
toms like  headache,  dizziness,  and  vomiting,  most  probably  through  an 
interference  with  the  general  circulation  of  the  brain.  Local  irritative 
symptoms  like  monospasms  and  unilateral  convulsions  form  by  no  means 
so  prominent  a  feature  of  acute  encephalitis  as  of  acute  meningitis,  and 
in  the  former  the  symptoms  which  indicate  a  general  compression  of  the 
brain,  such  as  somnolence  and  coma,  appear  at  an  earlier  period  than  in 
the  latter.  The  clinical  course  of  chronic  abscess  of  the  brain  is  similar 
to  that  of  an  intracranial  tumor,  and  the  symptoms  which  are  present 
in  the  former  depend  like  those  of  the  latter  upon  the  locality  of  the 
lesion. 

Treatment. — The  physician's  advice  may  be  sought  to  determine 
questions  of  cerebral  localization  and  other  delicate  points  of  diagnosis 
which  are  likely  to  arise  in  the  progress  of  abscess  of  the  brain,  but 
the  decision  with  regard  to  the  treatment  to  be  adopted  must  rest  with 
the  surgeon. 

The  secondary  inflammation  which  is  liable  to  supervene  in  the  course 
of  necrotic  softening,  cerebral  hemorrhage,  and  intracranial  tumors,  is 
the  form  of  encephalitis  which  is  most  likely  to  come  under  the  care  of 
the  physician.  This  form  of  encephalitis  is  best  treated  by  complete 
rest  in  a  darkened  room,  mild  purgation,  and  cold  applied  to  the  head. 
Active  measures  like  bleeding  and  blistering  are  worse  than  useless. 
In  chronic  abscess  of  the  brain  the  general  health  of  the  patient  must 
be  attended  to,  and  if  definite  localizing  symptoms  be  present  the  pus 
ought  to  be  removed  by  operation.  Paroxysms  of  severe  headache  may 
sometimes  be  relieved  by  chloride  of  ammonium,  while  more  active 
symptoms  like  delirium  may  be  combated  by  bromide  of  potassium, 
either  alone  or  in  combination  with  chloral,  and  an  opiate  or  cannabis 
indica  may  sometimes  be  found  useful. 


CHAPTER    XYII. 

ATROPHY,  HYPERTROPHY,  AND  TUMORS  OF  THE  BRAIN. 
I.  ATROPHY  OF  THE  BRAIN. 

1.  Atrophy  of  the  Corpus  Callosum. 

The  corpus  callosum  may  be  arrested  at  any  period  of  its  develop- 
ment so  that  it  may  be  entirely  wanting,  or  union  may  fail  to  take 
place  in  the  middle  line,  either  wholly  or  partially.  Deficiency  of  the 
corpus  callosum  has  generally  been  found  associated  with  idiocy  or 
imbecility,  but  the  mental  defects  do  not  present  anything  character- 
istic, and  some  cases  have  ])een  reported  in  which  there  was  no  mental 
defect,  and  consequently  the  condition  cannot  be  recognized  during  life. 

2.  Atrophy  of  the  Cerebellum. 

Atrophy  of  the  cerebellum  has  sometimes  been  met  with  as  a  primary 
disease  from  arrest  of  development,  but  atroj)hy  of  one  lateral  lobe  ol 
the  cerebellum  occurs  most  fre({uently  as  a  secondary  result  of  acquired 
atrophy  of  the  opposite  hemisphere  of  the  brain.  The  symptoms  most 
frequently  observed  in  the  primary  disease  are  a  staggering  gait,  along 
with  a  tendency  to  fall  backwards ;  persistent  or  temporary  disturbances 
of  speech ;  analgesia  and  other  sensory  disorders ;  epileptiform  convul- 
sions; and  weakness  of  mind,  or  idiocy. 

3.  Atrophy  of  the  Cerebral  Hemispheres. 

The  cerebral  hemispheres  are  arrested  in  their  development  in  cases 
of  microcephalic  and  other  forms  of  idiocy,  and  partial  defects  of  the 
brain,  either  from  arrest  of  development  or  from  destructive  lesions, 
are  met  with  in  parencephalus  and  unilateral  atrophy  of  the  brain, 
already  described  as  giving  rise  to  some  forms  of  the  spasmodic  paral- 
ysis of  infancy. 


IIYPERTEOPHY    OF    THE    BRAIX.  631 

II.  HYPERTKOPHY  OF  THE  BRAIN. 

1.  General  Hypertrophy  of  the  Brain. 

Etiology. — General  hypertrophy  of  the  brain  usually  appears  to  be 
congenital.  Several  of  the  reported  cases  were  associated  with  periph- 
eral multiple  neuroma,  and  both  of  these  conditions  are  frequent  accom- 
paniments of  idiocy  or  delayed  mental  development.  A  few  cases 
appear  to  have  developed  subsequently  to  an  injury  to  the  head,  while 
the  disease  appears  to  have  been  a  result  of  chronic  lead  poisoning. 

Symptoms. — The  symptoms  almost  always  appear  soon  after  birth  or 
in  early  infancy,  and  consist  of  epileptiform  convulsions,  local  spasms, 
attacks  of  laryngismus  stridulus,  and  tremors.  The  pulse  is  usually 
retarded,  but  it  may  occasionally  be  much  accelerated.  The  affection 
in  children  is  sometimes  associated  with  premature  development,  but 
in  other  cases  there  is  more  or  less  weakness  of  mind,  amountino; 
even  to  the  highest  degree  of  idioc3^  The  tongue  is  often  so  much 
increased  in  size  that  it  protrudes  from  the  mouth.  Drowsiness 
is  an  occasional  but  by  no  means  constant  symptom.  Some  of  the 
affected  children  are  liable  to  fall  fre({uently,  being  overbalanced  by  the 
great  weight  of  the  head.  Disturbances  of  the  nerves  of  the  general  or 
special  senses  are  comparatively  rare.  Death  results  from  •  an  attack 
of  convulsions,  from  cerebral  compression  with  coma,  or  from  an  inter- 
current disease. 

2.  Partial  Hypertrophy  or  Heterotopia  of  Brain  Substance. 

This  condition  was  first  described  by  Virchow,  and  has  hitherto  been 
principally  of  interest  to  the  morbid  anatomist.  Virchow  observed  in 
one  case  an  apparently  new  formation  of  gyri  within  the  white  sub- 
stance of  the  posterior  lobe,  and  a  hyperplastic  malformation  of  the 
caudate  nucleus,  while  Simon  met  with  small  accessory  gyri  on  the 
summit  of  the  convolutions.  Klob  found  a  mass  of  white  cerebral  sub- 
stance, the  size  of  a  bean,  hanging  from  a  pedicle  between  the  optic 
nerves. 

These  conditions  have  hitherto  been  found  in  epileptics,  idiots,  or  in 
persons  otherwise  mentally  affected,  but  their  clinical  significance  is 
somewhat  doubtful.  All  authors  regard  these  malformations  as  con- 
genital. ■ 


632      ATROPHY,  HYPERTROPHY,  AND  TUMORS    OF   BRAIN. 

III.  INTRACRANIAL  TUMORS. 

Etiology. — Tumors  of  the  brain  arise  from  similar  causes  to  those 
which  originate  tumors  in  other  localities,  and  these  need  not  be  de- 
scribed here. 

Symptoms. — Headache  is  one  of  the  earliest  and  most  striking  of 
the  initial  symptoms  of  intracranial  growths,  and  it  is  present  in  about 
two-thirds  of  all  cases.  The  headache  of  intracranial  tumor  consists 
of  an  acute  lancinating  or  severe  boring  pain  which  is  very  violent, 
and  may  continue  for  many  weeks  Avithout  intermission,  although  it  is 
liable  to  paroxysmal  exacerbations  of  great  severity.  The  pain  is 
aggravated  by  light,  noises,  and  all  movements  of  the  head,  and  it  may 
occupy  the  occipital,  frontal,  or  temporal  regions,  but  its  seat  has  no 
necessary  relation  to  the  situation  of  the  tumor.  The  skull  may,  how- 
ever, be  found  tender  to  percussion  at  a  point  corresponding  to  the 
situation  of  the  tumor.  The  profound  headache  of  cerebral  tumor  may 
also  be  accompanied  by  neuralgic  headache  caused  by  irritation  of  the 
fifth  nerve  in  its  course  along  the  base  of  the  brain.  The  pain  of 
trigeminal  neuralgia  occurs  in  paroxysms,  and  it  is  usually  associated 
with  numbness,  formication,  itching,  a  feeling  as  if  the  part  was 
swollen,  or  neuroparalytic  ophthalmia.  When  sensation  is  diminished 
on  the  painful  side,  or  when  all  three  branches  of  the  nerve  are  simul- 
taneously affected,  the  presence  of  tumor  may  be  suspected,  and  the 
diagnosis  is  rendered  more  certain  if  disorders  of  other  cranial  nerves 
are  present. 

Another  frequent  initial  symptom  of  intracranial  tumor  is  dizziness. 
which  may,  along  with  paroxysms  of  violent  headache,  be  the  only 
symptom  of  a  growth  which  presents  itself  for  many  months.  Vomit- 
ing is,  however,  apt  to  be  associated  with  headache  and  dizziness  in  the 
early  stages  of  a  cerebral  growth,  and  it  is  often  a  very  distressing 
symptom. 

Sensory  disorders  are  generally  ushered  in  by  liypemesthesia  or  some 
other  irritative  symptoms,  which  are,  after  a  time,  followed  by  anaes- 
thesia. Wandering  pains,  formication,  tingling,  and  numbness  alter- 
nate with  one  another  before  there  is  a  distinct  diminution  of  sensation, 
and  they  do  not  entirely  cease  until  complete  aniestliesia  is  established. 

The  motor  disorders  consist  at  first  of  tremor  of  one  extremity  or  of 
one-half  of  the  body,  or  of  cramps  which  may  vary  from  slight  spas- 
modic twitches  of  a  special  group  of  muscles  to  persistent  tonic,  clonic, 
or  choreiform  spasms  of  the  muscles  of  some  of  the  extremities.  The 
clonic  spasm  is  liable  to  assume  the  form  of  unilateral  epileptiform  con- 


INTRACRANIAL    TUMORS.  633 

vulsions  which  may  or  may  not  be  accompanied  by  unconsciousness. 
After  a  longer  or  shorter  time  the  irritative  motor  symptoms  give  place 
to  paralysis,  which  often  creeps  on  gradually  and  may  not  ])e  complete 
for  a  comparatively  long  time.  The  most  usual  form  of  paralysis  in 
cerebral  tumor  is  hemiplegia,  which  only  diifers  from  that  of  cerebral 
hemorrhage  by  the  fact  that  it  creeps  on  gradually  in  the  former,  instead 
of  being  suddenly  produced  as  in  the  latter,  and  that  the  spastic  con- 
dition of  the  limbs  is  not  generally  so  pronounced  in  the  hemiplegic 
tumor  as  in  that  of  hemorrhage. 

One  or  more  of  the  cranial  motor  nerves  may  be  compressed  at  the 
base  of  the  brain  or  at  their  point  of  origin  in  the  crus  cerebri,  pons, 
and  medulla  oblongata.  Paralysis  may  be  preceded  by  spasmodic 
twitchings  of  the  muscles  supplied  by  these  nerves. 

Various  forms  of  reeling  and  staggering  may  be  present  when  the 
tumor  is  situated  near  the  cerebellum  or  its  peduncles,  but  these  dis- 
orders belong  to  the  localizing  symptoms  and  will  be  subsequently 
described. 

The  sense  of  sight  is  frequently  affected  in  the  course  of  intracranial 
growths,  Calmeil  having  found  amblyopia  in  two-fifths,  and  Ladame 
amaurosis  in  one-fifth  of  the  cases  analyzed  by  them.  The  field  of 
vision  may  be  altered  in  various  ways  and  it  is  very  important  for 
regional  diagnosis  to  examine  for  the  diiferent  varieties  of  hemiopia. 
On  ophthalmoscopic  examination  the  fundus  of  the  eye  may  present 
the  usual  signs  of  optic  neuritis  or  of  the  "  choked  disk,"  the  latter 
being  by  far  the  most  important  sign  of  cerebral  tumor,  inasmuch  as  it 
is  seldom  present  except  when  the  intracranial  pressure  is  increased  in 
degree  by  a  solid  growth.  The  pupils  may  be  contracted  or  unequal, 
but  as  the  intracranial  pressure  becomes  great  by  the  increasing  size  of 
the  tumor  the  pupils  are  dilated  and  react  feebly  to  light. 

The  disorders  of  the  sense  of  hearing  consist  of  rustling  noises  in 
the  ears,  and  dulness  of  hearing,  but  complete  deafness  is  only  occa- 
sionally observed.  Paralysis  of  the  labyrinthine  fibres  of  the  auditory 
nerve  mav  cause  vertigo  and  motor  disorders  similar  to  those  observed 
in  Meniere's  disease. 

The  disorders  of  the  sense  of  sjnell  consist  of  subjective  sensations 
or  loss  of  smell  in  one  or  both  nostrils,  but  this  sense  is  not  often  affected. 

The  disorders  of  the  sense  of  taste  consist  also  of  subjective  sensa- 
tions or  loss  of  taste,  but  Ladame  found  that  this  function  was  only 
mentioned  as  having  been  affected  seven  times  out  of  all  the  cases  he 
had  collected. 

The  organic  functions  are  always  impaired  in  the  course  of  intra- 
cranial growths.     The  intense  headache  from  which  the  patient  suffers 


634      ATROPHY,  HYPERTROPHY,  AXU   TUMORS    OF   BRAIN. 

occasions  a  continued  wakefulness  which  reacts  upon  the  general  health, 
and  when  vomiting  recurs  frequently  the  general  nutrition  is  greatly 
impaired.  The  patient  often  suffers  from  constipation,  but  this  condition 
may  alternate  with  diarrhoea.  Polyphagia  is  an  occasional  symptom  of 
cerebral  tumor,  but  it  does  not  prevent  the  progressive  emaciation.  This 
symptom  is  occasionally  accompanied  by  diabetes  mellitus.  Polyuria 
with  or  without  saccharine  urine  is  not  an  infrequent  symptom  of  cerebral 
tumor.  In  the  early  stages  of  cerebral  tumor  the  action  of  the  heart 
may  be  irregular  and  slow  from  irritation  of  the  vagus,  but  towards  the 
end  the  pulse  becomes  extremely  frequent  from  ])aralysis  of  that  nerve. 
Respiration  is  not  often  affected,  but  its  rhythm  may  be  quickened  by 
irritation  and  rendered  slower  by  pressure  of  the  brain. 

Fever,  although  not  a  usual  symptom  of  cerebral  tum^or,  may  be 
present  during  complicating  attacks  of  encephalitis. 

The  psychical  disturbances  Avhich  are  present  in  greater  or  less 
degree  in  about  one-half  the  cases,  consist  at  first  of  mental  excitement 
and  emotional  displays  like  those  of  hysteria,  ideas  of  grandeur,  hallu- 
cinations, delusions,  and  outbursts  of  passion  which  may  amount  to 
maniacal  fury.  The  irritative  symptoms,  however,  give  place  after  a 
time  to  those  of  depression,  which  consist  of  drowsiness,  apathy,  loss  of 
speech,  and  imbecility.  The  terminal  symptoms  consist  of  extreme 
emaciation,  widely  spread  anaesthesia,  blindness  and  impairment  or  loss 
of  one  or  more  of  the  other  s|)ecial  senses,  motor  paralysis  which  often 
implicates  all  the  extremities,  imbecility,  and  deep  and  enduring  coma. 

Morbid  Anatomy. — The  morbid  anatomy  of  the  atrophy  and  hyper- 
trophy of  the  brain  is  a  wide  subject,  which  cannot  be  further  discussed 
here.  With  regard  to  intracranial  tumors,  it  Avill  suffice  to  remind  the 
reader  that  the  brain  is  surrounded  by  unyielding  osseous  walls  and 
that  consequently  all  growths  which  gradually  encroach  upon  the  space 
occupied  by  the  brain  must  give  rise  to  nearly  the  same  kind  of  symp- 
toms. The  tumors  themselves  being  so  variable  in  their  nature,  possess 
no  affinity  with  each  other  and  the  symptoms  to  which  they  give  rise 
from  their  situation  afford  the  only  grounds  for  grouping  them  together. 
Intracranial  tumors  may  be  divided  into,  </,  ncAV  formations  ;  6,  vascular 
tumors ;  and  c?,  parasites. 

Morbid  Physiology. — The  tumor  at  first  may  give  rise  to  few  or 
no  symptoms,  but  as  it  gradually  increases  in  volume  the  whole  brain 
is  subjected  to  pressure,  the  cerebro-spinal  fluid  is  first  displaced,  the 
blood  is  then  squeezed  out  and  the  whole  brain  becomes  anaemic ;  the 
functions  of  the  brain  become  gradually  diminished  aiul  ultimately  lost, 
and  the  patient  dies  comatose.  But  in  addition  to  this  general  pressure 
the  tissues  surrounding  the  growth  are  subjected  to  a  special  pressure 


INTRACEANIAL    TUMORS.  635 

Avbicli  soon  leads  to  their  destruction.  Destruction  of  tissue  is  at  other 
times  caused  by  ischaemic  softening  from  the  compression  of  an  artery, 
while  loss  of  function  may  be  caused  by  effusion  of  serum  from  com- 
pression of  veins.  But  although  the  direct  tendency  of  a  tumor  is  to 
destroy  the  surrounding  tissue,  its  indirect  effect  is  often  irritation,  and 
consequently  the  depression  symptoms  are  often  preceded  or  accompanied 
by  phenomena  of  irritation.  Still  greater  complications  in  the  symp- 
toms are  caused  by  the  fact  that  on  the  one  hand  irritation  of  a  higher 
centre  may  produce  an  inhibitory  action  on  a  lower  centre,  while  on  the 
other  hand  destruction  of  a  higher  centre  may  leave  the  functional 
activity  of  a  lower  centre  more  unrestrained.  The  symptoms  which 
are  caused  by  the  localization  of  the  tumor  do  not  differ  essentially  from 
those  caused  by  other  focal  diseases,  and  these  will  be  afterwards  con- 
sidered. The  intensity  of  the  symptoms  depends  to  some  extent  upon 
idiosyncrasies  of  the  patient,  the  locality  of  the  lesion,  and  in  still 
greater  degree  upon  the  rapidity  of  the  growth  of  the  tumor,  slow  grow- 
ing tumors  often  attaining  great  size  before  giving  rise  to  any  distinctive 
symptoms,  and  fast  growing  tumors  causing  very  active  symptoms  at  an 
early  period. 

Treatment. — In  the  earlier  stages  of  cerebral  tumors  the  symptoms 
of  irritation  and  local  congestion  predominate,  and  these  must  ])e  treated 
by  cold  to  the  head,  purgatives,  the  use  of  flying  blisters,  and  bromide 
of  potassium  either  alone  or  combined  with  chloral  hydrate.  The 
intense  headache  of  cerebral  tumor  must  be  treated  by  the  application 
of  cold  to  the  head,  and  subcutaneous  injection  of  morphia.  Chloride 
of  ammonium  in  half  drachm  doses  may  occasionally  be  found  useful. 
Epileptiform  convulsions  must  be  treated  by  large  doses  of  bromide  of 
potassium.  With  the  view  of  promoting  the  absorption  of  the  growth 
iodide  of  potassium  has  been  given  in  large  doses,  and  as  much  as  from 
half  a  drachm  to  a  drachm  may  be  given  three  times  a  day.  In  ])ro- 
gressive  growths  like  cancer,  sarcoma,  and  glioma  this  treatment  cannot 
of  course  lead  to  any  permanent  benefit,  but  it  may  be  useful  in  aneurism, 
and  is  by  far  the  most  hopeful  treatment  in  parasites.  If  syphilis  is 
suspected,  an  energetic  antisyphilitic  treatment  by  means  of  mercury 
and  iodide  of  potassium  must  be  undertaken.  It  is  possible  that  here- 
after surgeons  will  be  able  to  undertake  the  removal  of  a  considerable 
number  of  cerebral  tumors ;  even  already  a  few  successful  cases  have 
been  reported. 


V 


CHAPTER    XYIII. 

APHASIA. 

Aphasia  comprises  certain  disorders  of  the  faculty  of  language,  but 
inasmuch  as  every  form  of  disorder  is  not  to  be  included  under  the 
term  it  is  necessary  to  subject  the  faculty  itself  to  a  preliminary  analysis 
in  order  to  determine  which  belong  and  wliicli  do  not  belong  to  this 
group.  Language,  taken  in  its  evident  sense,  consists  of  the  various 
means  by  which  animals  indicate  mental  states  to  one  another,  this 
faculty  comprising  a  power  of  expressing  one's  own  states  and  of  ap- 
preciating the  states  of  others.  Mental  states  may  be  divided  into 
feelings,  cognitions,  and  volitions.  In  one  sense  language  may  be  said 
very  often,  if  not  always,  to  indicate  volitions,  but  inasmuch  as  volun- 
tary actions  are  always  determined  by  motives,  or,  in  other  Avords,  by 
the  feelings  and  cognitions,  the  language  of  volition  merges  into  that  of 
the  other  two  mental  states.  Language  may,  therefore,  be  divided  into 
that  of  the  feelings,  or  emotional  language,  and  that  of  the  cognitions, 
or  intdJectual  language,  or  speech.  The  distinction  between  the  lan- 
guage of  the  emotions  and  speech  is  by  no  means  clear  and  trenchant. 
When  a  man  delivers  an  oration,  for  instance,  only  a  small  part  of  his 
utterances  and  gestures  are  to  be  regarded  as  belonging  to  intellectual 
language.  All  the  variations  of  tone,  the  melodious  voice,  the  graces 
of  attitude  and  gesture,  the  charm  of  elegant  and  rhythmical  language, 
and  the  thousand  other  ways  by  which  a  great  orator  knows  how  to 
sway  and  influence  his  audience,  belong  to  emotional  and  not  to  intel- 
lectual language.  The  pleasure  we  derive  from  looking  at  a  clearly 
printed  volume,  and  especially  from  looking  at  an  illuminated  text,  or 
at  a  picture  rather  than  at  a  diagram,  shows  that  there  are  different 
means  whereby  the  feelings  may  be  engaged,  and  even  such  methods  as 
accents,  italics,  and  notes  of  exclamation,  by  means  of  which  inflection, 
emphasis,  and  wonder  are  indicated,  the  rhythm  of  metrical  language, 
and  the  diction  and  imagery  of  poetry,  all  belong  to  emotional  and  not 
to  intellectual  language.  The  language  of  emotional  and  of  intellectu.al 
gesture  are  also  by  no  means  readily  separated.  The  gestures  of  those 
who  retain  the  full  use  of  spoken  and  written  language  are  in  great  part 
indicative  of  the  feelings,  but  that  gestures  can  be  made  subservient  to 
intellectual  expression  is  shown  by  the  importance  it  assumes  in  the 


APHASIA.  637 

training  of  the  deaf  and  dumb.  But  although  it  is  not  always  easy  to 
discriminate  between  emotional  and  intellectual  language,  we  must 
repeat  that  it  is  disorders  of  speech  or  intellectual  language  alone  that 
are  comprised  under  the  term  aphasia. 

But  we  shall  now  see  that  aphasia  does  not  include  every  form  of 
disorder  of  intellectual  language.  Speech  is  the  instrument  of  the 
social  state,  and  that  it  may  be  the  means  of  communication  between 
animals  it  must  possess  to  each  a  subjective  and  an  objective  value,  or 
must  fulfil  an  impressive  and  an  expressive  function.  Each  individual 
of  a  social  community,  in  order  to  become  an  eftective  member,  must  be 
able  to  comprehend  the  mental  state  of  others  from  watching  their 
gestures  and  listening  to  their  various  vocalizations,  and  must  also  be 
able  by  his  gestures  and  vocalizations  to  render  his  own  mental  state 
intelligible  to  the  others.  The  subjective  or  impressive  function  of 
speech  may  be  divided  into  receptive  and  regulative  functions. 

The  receptive  department  is  represented  structurally  by  the  various 
peripheral  sense-organs  and  the  centripetal  fibres  Avhich  conduct  impres- 
sion upon  these  sense-organs  upwards  to  the  cortex  of  the  brain. 
Complete  loss  of  speech  from  disease  of  the  receptive  apparatus  is 
unknown.  The  vocal  speech  of  a  person  born  blind  is  almost  entirely 
unaffected  either  in  its  subjective  or  objective  aspects,  while  the  patient 
may,  by  the  device  of  raised  letters,  be  taught  to  understand  wa-itten 
language.  The  deaf-mute  is  taught  both  to  understand  and  to  give 
expression  to  a  complicated  speech  by  gestures,  and  in  recent  times 
such  patients  have  been  taught  not  only  to  use  their  vocal  organs  for 
expression  in  speech,  but  also  to  understand  the  vocal  speech  of  others 
by  closely  observing  the  movements  of  the  muscles  of  articulation. 

The  structural  counterpart  of  the  regulative  function  consists  of 
that  part  of  the  cortex  of  the  brain  in  which  the  centripetal  impulses 
are  reduced  to  such  order  as  is  necessary  to  render  them  the  corre- 
latives of  the  cognitions.  Now^  the  cognitions  express  the  relations 
between  our  feelings,  and  every  cognition  must  be  expressed  in  a 
proposition.  The  mode  of  expression  may  not  always  assume  a  distinct 
prepositional  form,  but  it  must  at  least  possess  a  prepositional  value  if 
it  convey  distinct  knowledge.  If  I  pronounce  the  word  "orange"  in 
the  hearing  of  another,  it  may  or  may  not  convey  to  him  distinct  in- 
formation, but  if  any  information  be  imparted  the  word  must  convey  to 
the  listener  the  idea  that  the  object  named  "orange"  belongs  to  a  class 
of  objects  already  known  to  him  under  that  name,  and  the  word  in  this 
sense  possesses  the  value  of  a  distinct  proposition.  If  the  listener  has 
never  had  any  experience  with  the  object  named  "orange,"  it  is  clear 
that  the  utterance  of  the  name  Avill  convey  no  meaning,  but  if  he  has 


638  APHASIA. 

liad  experience  of  fruits  and  colors,  distinct  information  may  be  con- 
veyed to  him  with  regard  to  the  object  by  saying  "an  orange  is  a 
yellow  fruit."  The  listener  will  be  able  to  associate  the  general  prop- 
erties of  fruit  and  a  distinct  color  with  the  Avord  in  future,  but  the 
information  has  been  imparted  by  means  of  a  formal  proposition.  The 
activity  of  the  regulative  cortical  centres  of  speech  has  for  its  func- 
tional correlative  the  arrangement  of  the  prescntative  and  representa- 
tive cognitions  into  the  form  of  distinct  mental  propositions. 

The  objective  or  expressive  function  of  speech  may  be  divided  into 
emissive  and  executive  departments. 

The  emissive  department  is  represented  structurally  by  that  organiza- 
tion in  the  cortex  of  the  brain  in  which  the  regulative  impulses  are 
finally  coordinate  before  being  conducted  to  tlie  executive  department. 

The  executive  department  is  represented  structurally  by  groups  of 
nerve  cells  in  the  central  gray  tube,  and  by  the  nerves  and  muscles 
concerned  in  vocalization,  articulation,  the  manual  operations  of  Avriting, 
and  various  gestures.  Complete  loss  of  speech  from  disease  of  the 
executive  apparatus  is  probably  unknown.  The  patient,  for  instance, 
may  lose  his  voice  in  different  diseases  of  the  larynx,  but  he  can  still 
articulate ;  he  may  lose  both  voice  and  power  of  articulation  in  bulbar 
paralysis,  but  he  is  generally  able  to  make  his  wants  known  in  writing, 
and  when  unable  to  write  from  want  of  a  previous  education,  he  can 
make  his  ordinary  recjuirements  known  by  gesture. 

Our  further  remarks  must  be  limited  to  the  derangements  of  speech 
caused  by  disease  of  the  cortex  of  the  brain,  and  which  are  grouped 
together  under  the  name  of  aphasia.  These  disorders  consist  of  affec- 
tions of  the  regulative  department  of  the  impressive  function,  and  of 
the  emissive  department  of  the  expressive  function  ;  the  former  of  these 
being  named  sensory  and  the  latter  motor  aphasia.  In  addition  to  these 
two  chief  varieties  there  are  cases  in  which  the  ingoing  and  outgoing 
functions  of  speech  are  both  affected,  and  inasmuch  as  the  lesion  in  such 
cases  is  situated  between  the  sensory  and  motor  cortical  centres  Wernecke 
proposes  to  group  them  under  the  name  of  commissural  aphasia,  but 
here  Ave  shall  treat  of  them  under  the  name  of  )tnxed  sensory  and  motor 
aphasia.  As  motor  aphasia  is  the  simplest  form  of  the  affection,  we  shall 
deal  with  it  first. 

MOTOR  APHASIA. 

In  cases  of  motor  aphasia  the  patient  is  unable  to  communicate  his 
thoughts  by  words  (motor  aphemia),  or  by  writing  (motor  agraphia), 
wliile  there  is  loss  or  impairment  of  his  intellectual  pantomime  (motor 


MOTOR    APHASIA.  039 

amimia).  The  patient  can  often  utter  words,  but  they  do  not,  if  the 
motor  aphasia  is  complete,  possess  any  intellectual  value  ;  in  the  lanffuao-e 
of  Dr.  Hughlings-Jackson,  the  patient  is  speechless  but  not  wordless. 
The  words  which  the  patient  can  utter  continue,  as  a  rule,  the  same  for 
the  same  patient — "  recun-ing  utterances,"  or  the  patient  may  under 
excitement  swear,  or  even  utter  a  phrase  appropriate  to  the  surroundino- 
circumstances,  such  as  "  good-bye  "  when  a  friend  is  leaving.  It  will 
be  readily  seen  that  "■  recurring  utterances"  like'"  yes  "  and  "  no," 
Avhich  are  repeated  on  all  occasions  whether  appropriate  or  not,  do 
not  possess  any  intellectual  value,  while  of  the  occasional  utterances 
swearing  is  a  purely  emotional  expression,  and  even  the  phrase  "  o-ood- 
bye"  must  be  regarded  as  expressing  a  state  of  mental  regret  rather 
than  a  purely  intellectual  appreciation  of  the  surrounding  conditions. 
In  some  cases,  in  addition  to  the  usual  recurring  utterances  of  "yes" 
and  "  no,"  the  patient  repeats  such  phrases  as  "  come  on  to  me,  '  or 
"  I  want  protection."  The  man  whose  recurring  utterance  was  "  come 
on  to  me  "  was  a  railway  signalman,  and  had  been  taken  ill  on  the  rails 
in  front  of  his  box,  while  the  man  who  could  only  say  "  I  Avant  protec- 
tion," had  his  left  cerebral  hemisphere  injured  in  a  brawl.  Dr.  Hughlings- 
Jackson  makes  the  very  probable  supposition  that  in  these  cases  the 
recurring  utterances  constituted  the  last  words  spoken,  or  which  were  in 
a  state  of  mental  preparation  for  utterance  when  the  damage  occurred 
to  the  brain.  It  is  not  improbable  that  words  uttered  or  about  to  be 
uttered  during  a  period  of  great  excitement  may  leave  permanent 
traces  on  the  ororanization  of  the  brain  which  will  render  them  liable 
to  be  subsequently  uttered  as  interjectional  phrases  during  emotional 
states.  That  all  these  words  and  phrases  must  be  regarded  as  expressive 
of  emotional  rather  than  intellectual  states  is  shown  by  the  fact  that  the 
patient  is  frequently  unable  to  repeat  his  favorite  oath  or  his  formula  of 
leave-taking,  or  perhaps  "  yes  "  or  "  no,"  when  asked  to  do  so. 

The  patient  is  not  always  completely  speechless  ;  he  may,  for  instance, 
retain  the  full  use  of  the  words  "  yes  "  and  "  no,"  and  even  when  he 
uses  "  no  "  to  express  assent  as  well  as  dissent  he  may  be  able,  by  the 
aid  of  pantomime,  to  make  it  known  in  which  sense  he  intends  the  word 
to  be  understood.  All  forms  of  intellectual  expression  are  not  affected 
to  the  same  degree.  A  patient  may  have  lost  the  use  of  vocal  speech 
completely  and  yet  retain  to  a  greater  or  less  extent  the  power  of 
writing,  and  conversely  a  patient  may  retain  or  reacquire  the  full  use  of 
vocal  speech  while  the  power  of  writing  is  permanently  lost ;  in  other 
Avords,  motor  aphemia  may  be  present  without  agraphia,  or  agraphia 
without  aphemia.  The  fliculty  of  intellectual  pantomime  is  also  often 
reacquired  long  before  that  of  vocal  speech  in  cases  of  motor  aphasia ; 


640  APHASIA. 

but  none  is  known,  so  far  as  I  am  aware,  in  wliich  the  former  was  per- 
manently lost  while  the  latter  was  regained. 

In  motor  aphasia  the  patient  understands  all  that  is  said  to  him  and 
remembers  what  is  read  to  him  or  what  he  reads  himself;  his  vocal 
organs  act  normally  ;  the  muscles  of  mastication  and  deglutition  are  not 
paralyzed,  and  he  can  sing,  laugh,  smile,  and  frown  as  usual.  He 
will  point  to  objects  named  and  recognize  drawings  of  them,  provided 
they  were  known  to  him  before  his  illness.  He  is  able  to  play  at 
cards  and  other  games,  and  recognizes  handwriting.  He  can  copy 
Avriting,  provided  his  hand  is  not  paralyzed,  but  in  aggravated  cases  the 
patient  copies  printed  words  in  printed  characters  and  written  words  in 
written  characters.  If  the  right  hand  is  paralyzed,  the  patient  on 
attempting  to  use  his  left  hand  Avrites  from  right  to  left  instead  of  from 
left  to  right  as  usual,  the  result  being  Avhat  is  known  as  "  mirror-writ- 
ing," so  named  because  it  looks  like  ordinary  writing  only  on  being 
reflected  from  a  mirror. 


SENSORY   APHASIA   (AMNESIC   APHASIA). 

The  purest  examples  of  sensory  aphasia  consist  of  the  aftections 
known  as  word-hlindiicss  and  word-deaf nesx. 

In  word-blindneas  the  patient  is  totally  unable  to  comprehend  written 
or  printed  language,  but  he  is  at  the  same  time  not  blind,  inasmuch  as 
he  avoids  obstacles  in  walking,  and  takes  notice  of  everything  that 
passes  around  him.  His  sight  is,  however,  sometimes  defective,  right- 
sided  bilateral  homonymous  hemianopia  being  often  if  not  always  present, 
but  this  defect  does  not  prevent  the  patient  from  reading  fairly  well 
when  the  lesion  is  situated  in  the  optic  tract.  The  patient  can  write 
spontaneously  or  to  dictation,  but  he  cannot  copy  printed  or  written 
words  and  is  quite  unable  to  read  what  he  has  himself  just  written. 
The  patient  is  not  only  totally  unable  to  read  aloud,  but  singularly 
enough  he  may  also  be  quite  unconscious  of  his  disability.  A  patient 
of  mine  on  being  presented  with  a  letter  which  I  had  just  received 
making  in(|uiries  about  a  patient  attending  as  an  out-patient  at  the 
infirmary,  read  without  much  hesitation  :  "  Manchester  Royal  Infirmary. 
Dear  Sir :  You  are  requested  to  bring  this  paper  with  you  the  next 
time  you  come  to  the  Infirmary."  Not  a  single  word  of  this  corre- 
sponded with  the  note  which  he  pretended  to  read.  His  wife  told  me 
that  at  home  he  pretended  to  read  the  newspaper  aloud,  but  she  added 
"it's  all  stufi"  out  of  his  own  head."  One  night  he  stopped  in  the 
midst  of  a  paragraph  in  which  he  was  apparently  interested  ami  asked 


I 


SENSORY    APHASIA.  (Ul 

his  Avife  to  finish  the  remainder  of  it.  She  read  the  paragraph  aloud 
as  it  was  printed,  and  in  great  surprise  he  asked,  "  Is  that  what  it  says  ?  " 
and  on  being  assured  that  such  was  the  case  he  added,  "  Well !  I  must 
be  an  idiot." 

In  ivord-deafness  the  patient  is  unable  to  understand  the  vocal  speech 
of  others.  The  subjects  of  this  disorder  hear  as  Avell  as  ever  a  knock- 
ing at  the  door  or  the  tick  of  a  watch,  but  are  totally  unable  to  com- 
prehend the  language  of  others,  or,  in  other  words,  spoken  words  fail  to 
call  up  in  the  mind  of  the  patient  the  images  correspondino-  to  the 
persons,  things,  events,  and  relations  indicated  by  the  words.  When 
word-deafness  is  complete,  the  subject  of  it  fails  to  do  anything  requested 
of  him.  But  even  in  such  cases  the  patient  is  quick  at  interpretino- 
signs,  and  if  the  physician  ask  him  to  put  out  his  tongue  he  may  do  so 
not  because  he  understands  the  spoken  request,  but  because  he  notices 
that  the  eyes  of  the  observer  are  directed  to  his  mouth.  In  most  cases, 
however,  the  disorder  is  partial,  and  the  patient  is  then  able  to  compre- 
hend ftimiliar  words  and  phrases,  and  may  put  his  tongue  out,  close  the 
door,  and  perform  a  number  of  other  simple  and  common  actions  when 
asked.  A  very  good  test  of  word-deafness  is  the  one  proposed  by  Dr. 
Hughlings-Jackson,  namely:  Ask  the  patient  some  absurd  question, 
such  as  "Are  you  a  hundred  years  of  age?"  If  the  patient  compre- 
hends the  question  it  will  excite  astonishment  and  amusement.  A  patient 
of  mine  when  asked  the  question  says  readily,  "No,  I  don't  think  I  am 
so  old  as  that,"  and  evidently  the  question  does  not  cause  him  any  sur- 
prise, but  when  100  is  presented  to  him  in  written  figures  he  then 
bursts  into  laughter  and  says,  "Pooh!  Nothing  like  it." 

Word-deafness  is  almost  always  associated  with  a  certain  degree  of 
word-blindness.  Speech  is  organized  for  the  first  time  in  connection 
with  the  sense  of  hearing,  and  when  some  time  afterwards  written  speech 
comes  to  be  organized,  the  visible  characters  are  understood  through  the 
medium  of  the  already  organized  audible  characters.  The  connection 
between  the  written  and  spoken  words  varies  greatly  in  difterent  cases. 
In  uneducated  persons  written  speech  is  only  understood  by  being  read 
aloud  or  translated  into  spoken  speech,  and  in  such  cases  word-deafness 
would  entail  complete  word-blindness.  Educated  persons,  however, 
understand  the  meaning  of  written  words  directly,  so  that  injury  of  the 
auditory  centre  would  not  damage  much  the  understanding  of  written 
speech.  A  patient  of  mine,  who  has  received  a  tolerable  education,  is 
suffering  from  word-deafness,  and  he  can  read  aloud  without  committing 
many  mistakes,  while  he  apparently  understands  what  he  reads,  but  he 
is  unable  to  name  a  single  object  presented  to  him.  The  sight  of  the 
object  does  not  call  up  its  name,  and  yet  there  is  every  ground  for  be- 

41 


642  APHASIA. 

lieving  that  the  lesion  is  situated  in  the  auditory  cortical  centre,  and 
that  the  visual  centre  is  free  from  disease.  In  this  case  the  patient  is 
totally  unable  to  name  his  own  fingers,  but  when  the  word  is  written 
down  he  immediately  identifies  it  as  indicating  the  finger  of  his  own 
hand.  Another  patient  with  hemiopia  and  word-blindness,  fails  to  rec- 
ognize the  written  word,  but  readily  names  his  finger  or  any  other 
object  when  presented  to  him.  The  disorder  of  the  expressive  faculty 
of  speech  in  word-deafness  is  (piite  as  interesting  as  the  disorders  of  the 
impressive  faculty.  When  the  patient  speaks  he  misplaces  words,  as 
calling  the  "window"  a  "fender,"  or  he  uses  a  word  kindred  in  its 
meaning  with  the  one  intended,  as  "Avorm  powder"  for  "cough  medi- 
cine," or  in  its  sound,  as  "parasol"  for  "castor  oil."  This  condition, 
which  has  Ijeen  named  by  Kussmaul  paraphasia,  may  be  present  in 
word-blindness  as  well  as  in  word-deafness,  and  possibly  also  in  the 
incomplete  form  of  motor  aphasia.  A  condition  Avhich  may  be  named 
paragraphia  is  also  often  present. 

A  patient  of  mine  on  being  asked  to  write  his  own  name,  "William 
Abson,"  wrote  down  "Wuagageag  Abreaghrer,"  and  on  being  asked 
to  copy  a  passage  beginning  "with  deep  feeling,"  he  wrote  with  great 
care  and  deliberation,  and  in  a  good  hand,  "weeth  deap  flneearer." 
As  the  patient  wrote  each  letter  he  named  one  aloud,  but  the  written 
and  spoken  letter  never  corresponded  with  one  another.  AVhen  asked 
to  read  a  passage  beginning  with  "Oh,  those  dreams  of  my  childhood 
and  my  youth,"  he  read  "On  througli  depth  of  my  shouded  and  my 
youth."     This  condition  has  been  called  para?('«/a. 

A  profounder  degree  of  disorder  than  paraphasia  is  found  in  those 
cases  just  mentioned,  in  which  the  presentation  of  persons  and  things 
to  the  patient  fails  to  call  up  their  names.  The  patient  already  men- 
tioned as  being  unable  to  name  his  own  finger,  has  only  the  use  of 
three  or  four  concrete  nouns,  which  he  employs  on  all  occasions,  yet 
he  has  a  large  vocabulary  of  words  expressive  of  events,  dates,  and 
relations,  as  well  as  the  use  of  some  abstract  nouns.  On  being  pressed 
for  the  name  of  his  thumb,  he  called  it  "the  public  house,"  the  index 
finger  "the  first  one,"  and  on  being  pressed  still  further  for  a  name, 
"the  first  halfpenny;"  the  middle  finger,  "the  second  halfpenny;"  the 
ring  finger,  "threepence;"  and  the  little  finger,  "the  fourth  half- 
penny." Asked  the  name  of  a  watch,  he  called  it  "a  glass  of  beer," 
and  to  indicate  his  appreciation  of  the  diff'erence  between  a  gold  and 
silver  watch  presented  to  him,  he  pointed  to  the  first  as  being  "the  best 
beer."  The  only  names  of  things  in  his  possession  are  public  house, 
glass  of  beer,  and  the  names  of  the  coins  in  ordinary  circulation,  but 
which   he  seldom  uses  correctly.     He  can   count  up  to  any  number 


i 


MIXED    MOTOR    AND    SENSORY    APHASIA.  643 

when  he  begins  from  one,  but  it  is  only  on  rare  occasions  that  he  is 
able  to  break  in  on  the  series  and  begin  Avith,  say  six.  This  patient  is 
almost  completely  word-deaf,  but  will  show  his  appreciation  of  most 
requests  and  statements  made  in  writing.  A  still  more  aggravated 
disorder  of  the  expressive  faculty  of  speech  is  found  in  those  cases  in 
which  the  vocal  speech  of  the  patient  is  an  unintelligible  jargon.  Such 
patients  fail  to  comprehend  either  written  or  spoken  language,  and  it  is 
probable  that  the  sensory  aphasia  is  also  accompanied  by  a  motor 
aphasia.  A  patient  of  mine  takes  a  book  in  his  hand  and  begins  to 
read  aloud  with  much  apparent  relish,  and  uses  variations  of  accent, 
inflection,  and  pauses  to  give  emphasis  to  his  reading,  but  his  vocaliza- 
tions are  quite  unintelligible,  and  consist  of  such  sounds  as  "pluf,  plon, 
lep,"  etc.  The  intervals  between  his  pauses  seem  to  depend  upon  his 
breathing  capacity,  and  to  have  no  relation  to  the  length  of  the  sen- 
tences on  the  printed  page  before  him.  When,  however,  the  page  is 
presented  to  him  upside  down  he  immediately  turns  it  the  right  side  up, 
and  Avith  an  expression  of  great  impatience. 


MIXED   MOTOR   AND   SENSORY   APHASIA. 

In  cases  of  right-sided  hemiplegia  Avith  aphasia  the  patient  is  fre- 
quently unable  either  to  express  a  single  word  or  to  comprehend  any 
question  addressed  to  hiui  in  Avritten  or  spoken  language.  There  is  at 
first  total  motor  aphasia  and  total  sensory  aphasia.  In  cases  of  this 
kind,  however,  gradual  recovery  takes  place,  and  after  a  time  either  the 
motor  or  the  sensory  aphasia  greatly  diminishes  or  Avholly  disappears. 
A  young  boy  Avas  recently  under  my  care  Avho,  after  an  attack  of  right- 
sided  hemiplegia,  sufiered  from  complete  motor  and  sensory  aphasia. 
The  presence  of  a  systolic  murmur  at  the  apex  of  the  heart  showed 
that  the  apoplectic  attack  which  caused  the  paralysis  was  of  embolic 
origin.  After  a  time  a  gradual  improvement  took  place  ;  the  patient 
began  to  obey  such  ordinary  requests  as  "put  out  your  tongue,"  and 
"  close  your  eyes,"  and  a  few  months  after  the  attack  the  sensory  aphasia 
completely  disappeared,  and  only  slight  traces  of  the  hemiplegia  could 
be  detected,  but  the  motor  aphasia  still  persists  six  months  after  the 
attack.  In  some  cases  of  this  kind  the  improvement  appears  to  take 
place  on  the  motor  side.  Those  aggravated  cases  of  word-deafness 
and  word-blindness  in  which  the  speech  is  mere  jargon  are  fre(|uently 
if  not  always  accompanied  by  hemiplegia,  and  in  such  cases  the  motor 
as  well  as  the  sensory  aphasia  is  at  first  more  or  less  complete,  and 
even  when  partial  recovery  takes  place  it  is  probable  that  these  cases 


644  APHASIA. 

are  to  be  recognized  as  a  mixed  motor  and  sensor}'-,  rather  than  a  pure 
sensory  aphasia. 

Morbid  Anatomy  and  Physiology. — The.  faculty  of  language  was 
placed  by  Gull  in  the  supra-orbital  lobes  of  the  brain,  but  the  first 
serious  attempt  to  determine  the  localization  of  this  faculty  by  means  of 
morbid  anatomy  was  made  by  Bouillaud,  who,  in  1825,  came  to  the 
conclusion  that  the  faculty  of  speech  was  situated  in  the  anterior  cerebral 
lobes.  In  1836,  Marc  Dax  advanced  the  opinion  that  the  organ  of 
language  was  situated  in  the  left  hemisphere  of  the  brain  near  to  the 
Island  of  Riel,  but  this  opinion  was  neglected  and  almost  forgotten 
until  1861,  when  Broca  localized  the  faculty  of  language  in  the  third 
left  frontal  convolution.  In  the  subsequent  two  years  Broca  collected 
seventeen  cases  of  aphasia  with  post-mortem  examinations,  and  of  these 
the  lesion  Avas  situated  sixteen  times  in  the  posterior  part  of  the  third 
left  frontal  convolution  and  once  in  the  temporal  lobe  and  Island  of  Riel. 
Soon  afterwards  cases  were  published  by  Parrot,  Fernet,  and  Charcot, 
in  which  a  destructive  lesion  of  the  jiosterior  part  of  the  third  right 
frontal  convolution  had  not  given  rise  to  any  disorder  of  speech,  these 
cases  affording  the  negative  side  of  the  proof  that  the  faculty  of  language 
is  organized  in  the  left  hemisphere.  It  was  suggested  by  Bouillaud  and 
Broca  that  the  faculty  of  speech  is  organized  in  the  same  hemisphere 
of  the  brain  as  the  mechanism  which  regulates  the  special  movements  of 
the  hand,  and  in  proof  of  this  supposition  it  has  been  found  tliat  aphasia 

Fia.  17(1. 


does  coexist  with  left-sided  hemiplegia  in  left-handed  people,  several 
cases  of  this  kind  being  now  recorded  by  different  observers.  The  lesion 
in  aphasia  may  consist  of  a  growth,  of  a  depressed  bone,  or  of  a  hemor- 
rhage, but  occlusion  of  the  Sylvian  artery  or  of  one  of  its  branches  is 
by  far  the  most  frequent  cause  of  aphasia. 


MOKBID    ANATOMY, 


645 


Lesions  of  the  centrum  semiovale  which  damage  the  fibres  of  the 
corpus  callosum  Avhich  connect  the  third  frontal  convolutions  of  the  two 
hemispheres,  and  the  fibres  which  connect  the  third  left  frontal  convolu- 
tion with  the  internal  capsule,  occasion  an  aphasia  which  is  as  permanent 
as  that  caused  by  destruction  of  Broca's  convolution  itself  (Fig.  176,  L). 
In  sensory  aphasia  the  lesion  is  localized  in  the  area  of  distribution  of 
the  parieto-sphenoidal  and  sphenoidal  branches  of  the  Sylvian  artery 
(Fig.  177,  4  and  5).     In  Avord-deafness  the  lesion  is  situated  in  the  first 

Fig.  177. 


Diagram  Showing  the  Area  of  Distribution  of  the  Middle  Cerebral  Artery. 
S,  Sylvian  or  middle  cerebral  arterj' ;  P,  Perforating  branches ;  1,  Inferior  frontal  branch  ;  2,  Ascending 
frontal  branch  ;  ?•,  Ascending  parietal  branch  ;  4  and  5,  Parieto-sphenoidal  and  sphenoidal  branches;  A, 
Ascending  frontal  convolution;  B,  Ascending  parietal  couvolntion ;  Fj,  Fo,  Fj,  First,  second,  and  third 
frontal  convolutions ;  Pj,  Po,  P3,  First,  second,  and  third  parietal  convolutions ;  Tj,  To,  T3,  First,  second, 
and  third  temporo-sjihenoidal  convolutions  ;  OL,  Occipital  lobe. 

and  second  temporo-sphenoidal  convolutions  (the  acoustic  centre),  and 
in  word-blindness  in  the  angular  gyrus  and  adjacent  parts  of  the  occipital 
lobe  (the  visual  centre).  The  shaded  portion  in  Fig.  178  shows  the 
position  of  the  lesion  in  a  case  of  word-deafness  reported  by  Wernicke. 
The  lesion  may  also  be  situated  in  the  white  substance  subjacent  to 
these  convolutions.  In  mixed  sensory  and  motor  aphasia  the  Sylvian 
artery  is  occluded  immediately  outside  the  nutritive  arteries  which  pass 
into  the  anterior  perforated  space,  and  consequently  the  circulation  is 
arrested  through  all  the  cortical  branches  of  the  vessel.  The  result  of 
occlusion  of  the  vessel  at  this  point  is  that  hemiplegia  is  associated 
with  aphasia,  and  the  sensory  as  well  as  the  motor  centres  are  partially 


646 


APHASIA. 


damaged.  It  must,  however,  be  remembered  that  the  temiinal  cortical 
branches  of  the  Sylvian  artery  anastomose  to  some  extent  with  the 
terminal  branches  of  the  anterior  and  posterior  cerebral  arteries,  and 
occlusion  of  the  vessel  is  not  always  followed  by  extensive  softening, 
especially  in  young  people.  A  young  girl  came  under  my  observation 
who  was  suffering  from  mitral  disease,  and  who  died  a  fortnight  after 
an  attack  of  right-sided  hemiplegia  with  complete  motor  and  sensory 
aphasia.  At  the  autopsy  an  embolus  was  discovered  in  the  left  Sylvian 
artery  immediately  outside  the  nutritive  arteries  to  the  anterior  per- 

FiG.  178. 


forated  space,  but  not  a  trace  of  softening  could  be  discovered  in  the 
hemisphere.  The  whole  brain  was  very  amemic  and  the  cortex  of  the 
left  hemisphere  was  particularly  pale,  and  it  is  probable  that  the  cells 
had  undergone  fattv  degeneration,  but  there  was  no  .softening,  and  it  is 
possible  that  had  the  patient  lived  the  cortex  of  the  central  convolutions 
would  have  completely  recovered.  In  older  people,  however,  softening 
of  some  portion  of  the  cortex  always  takes  ])lace  after  occlusion  of  the 
Sylvian  artery.  The  softening  may  sometimes  take  place  in  the  area 
of  the  posterior,  and  more  frequently  in  the  area  of  the  anterior 
branches,  while  at  times  the  intt-rvening  portion  of  the  cortex  is  more 
or  less  disorganized,  and  thus  it  is  that  a  disorder  of  speech  which  at  first 
is  a  complete  motor  and  sensory  aphasia  may  recover,  so  that  it  becomes 
a  simple  motor  or  a  simple  sensory  aphasia,  according  to  the  locality 
which  is  permanently  softened,  or  may  remain  permanently  a  combined 
motor  and  sensory  aphasia  in  case  a  wide  area  of  the  cortex  undergoes 
softening. 

Motor  aphemia  is  caused  by  destruction  of  the  posterior  part  of  the 
third  left  frontal  convolution  for  the  same  reason  that  paralysis  of  the 
right  hand  is  caused  by  destruction  of  the  ascending  frontal  and  parietal 


MORBID    ANATOMY.  647 

convolutions.  It  may  be  objected  that  in  motor  aphemia  the  muscles 
of  articulation  are  not  paralyzed,  inasmuch  as  there  is  no  sign  of  a  local 
paralysis  of  the  tongue  or  lips.  But  notwithstanding  that  the  general 
movements  of  the  tongue  and  lips  are  unaffected,  there  is  a  paralysis  of 
the  special  combination  of  muscular  movements  which  are  required  to 
produce  articulate  sounds,  and  in  motor  agraphia  there  is  a  paralysis  of 
the  particular  combination  of  movements  by  which  writing  is  effected, 
although  the  general  movements  of  the  hand  may  be  unimpaired.  The 
reason  that  motor  aphemia  and  agraphia  are  so  frequently  associated  is 
that  the  centre  for  the  special  movements  of  the  tongue  and  lips,  and 
that  for  the  special  movements  of  the  hand  lie  near  together;  the  one 
being  organized  in  the  posterior  portion  of  the  third  frontal  convolution, 
and  the  other  in  the  adjoining  inferior  part  of  the  ascending  frontal 
and  parietal  convolutions.  But  although  these  two  centres  lie  near 
together,  the  fact  that  they  still  form  separate  centres  explains  why 
it  is  that  the  one  kind  of  disorder  may  be  present  without  the  other, 
and  that  the  two  are  only  seldom  present  in  any  one  case  in  an 
equal  degree.  The  reason  that  the  general  movements  of  the  tongue 
and  lips  are  not  paralyzed  in  lesion  of  the  left  hemisphere  is  that  they 
are  organized  in  both  hemispheres,  and  that  when  the  organization  in 
the  left  hemisphere  is  destroyed  the  right  hemisphere  takes  up  the 
action  and  maintains  the  general  movements  of  both  sides.  It  may, 
therefore,  be  presumed  that  the  recurring  utterances  which  are  met 
with  in  cases  of  complete  motor  aphasia  are  also  like  the  general  move- 
ments of  the  tongue  and  lips,  organized  in  both  hemispheres  of  the 
brain.  But  if  motor  aphasia  is  caused  by  destruction  of  a  motor 
centre  in  the  cortex  of  the  left  hemisphere  of  the  brain,  why  is  it  that 
aphasia  is  not  caused  by  destruction  of  the  conducting  path  which  con- 
nects this  centre  with  the  bulbar  nuclei  ?  The  answer  is,  that  injury  of 
the  conducting  path  in  the  knee  of  the  internal  capsule  does  cause  an 
aphasia,  although  it  does  not  remain  permanent.  A  right-sided  hemi- 
plegia caused  by  hemorrhage  into  the  lenticular  nucleus  is  accompanied 
by  a  motor  aphasia  at  first,  but  the  disorder  of  speech  passes  off  in  a  few 
weeks  or  months  at  most.  The  explanation  which  Dr.  Broadbent  has 
given  of  this  fact  is  generally  accepted.  He  believes  that  when  the 
direct  conducting  path  which  connects  the  third  left  frontal  convolu- 
tion with  the  bulbar  nuclei  is  interrupted,  a  new  path  is  gradually 
opened  first  from  the  third  left  to  the  corresponding  third  right  frontal 
convolution,  through  the  corpus  callosum,  then  through  the  pyramidal 
tract  of  the  right  hemisphere  to  the  bulbar  nuclei.  But  when  the 
right  pyramidal  tract  is  injured  subsequently  to  an  injury  of  the  left 
tract,  there  not  only  is  then  more  or  less  aphasia,  but  the  general  move- 


648  APHASIA. 

ments  of  the  lips  and  tongue  become  paralyzed,  and  the  patient  presents 
all  the  phenomena  of  a  bulbar  paralysis.  But  if  motor  aphasia  is  a 
paralysis  of  certain  special  movements,  we  shall  now  see  that  sensory 
aphasia  is  an  anaesthesia  to  certain  properties  of  matter,  while  the  ap- 
preciation of  the  general  properties  is  retained.  The  condition  of 
patients  who  are  word-deaf  and  word-blind  is  comparable  to  the  mental 
state  to  which  Goltz  reduced  dogs  by  washing  out  lai-ge  portions  of  the 
cortex  of  the  brain.  The  animal  operated  upon  recovers  to  a  greater 
or  less  extent  from  the  paralysis  which  follows  immediately  upon  the 
injury,  but  it  is  found  that  the  psychical  capacity  is  very  seriously  im- 
paired. He  is  not  blind,  because  in  walking  about  the  laboratory  he 
avoids  obstacles,  but  he  fails  to  recognize  his  usual  food  as  such,  and 
the  vessel  in  which  it  is  contained  is  avoided  as  an  obstacle. 

The  (log  still  retains  the  knowledge  which  connects  the  falling  of  a 
shadow  upon  the  eye  with  the  near  proximity  of  a  resisting  body,  which 
is  the  most  general  of  all  knowledge,  but  he  has  lost  the  knowledge  which 
is  only  a  little  less  general  tlian  it,  that  a  particular  substance  possesses 
the  specific  properties  of  taste  and  smell,  which  constitutes  its  food  to 
be  eaten  and  not  an  obstacle  to  be  avoided.  On  the  side  of  the  audi- 
tory sense  the  dog  is  equally  deficient;  he  is,  indeed,  like  the  word- 
deaf:  he  still  hears  noises,  but  fails  to  respond  to  his  own  name.  'J'o 
make  the  similarity  between  the  dogs  operated  upon  by  (loltz  and  the 
word-deaf  and  word-blind  more  complete,  a  post-mortem  examination 
of  the  dog  exhibited  at  the  International  Medical  Congress  at  London, 
showed  that  the  cortex  was  chiefly  injured  in  the  occipital  and  temporo- 
sphenoidal  lobes,  or  in  the  sensory  areas  of  the  cortex.  A  more  or  less 
similar  mental  condition  to  that  of  the  dog  operated  upon,  so  far  as 
regards  sight,  was  observed  by  Fiirstner  in  cases  of  general  paralysis 
of  the  insane,  in  which  the  occipital  lobes  were  specially  involved  in 
the  disease.  The  patient  could  still  see  large  objects  and  avoid  them 
as  obstacles,  but  was  unable  to  count  correctly  small  objects,  and  lost 
all  knowledge  of  the  special  properties  of  matter.  A  coin,  for  instance, 
he  recognized  as  made  of  metal,  and  as  liaving  a  certain  form  and  size, 
but  he  had  no  knowledge  of  the  special  properties  which  gave  it  value 
as  a  money  tender.  The  word-deaf  and  tlie  word-blind  are  not  reduced 
to  so  low  a  condition  of  intelligence  as  this,  but  their  disability  is  the 
same  in  its  essential  features ;  there  is  a  loss  of  the  more  special  and 
least  organized  knowledge,  and  a  preservation  of  the  more  general  and 
best  organized  knowledge.  To  elaborate  this  idea  would  reijuire  much  more 
time  and  space  than  1  can  aflbrd,  but  it  will  suffice  to  say  that,  speaking 
generally,  the  best  organized  knowledge  is  that  which  is  most  frequently 
repeated  in  the  experience  of  any  individual,  and  of  the  race.     As  I 


MORBID    ANATOMY.  649 

look  around  me,  I  see  a  number  of  objects  which  I  recognize  as  books, 
and  one  would  think  that  the  association  between  the  sight  of  a  book 
and  its  name  is  well  organized  in  me,  and  so  no  doubt  it  is.  But  of 
each  book  I  can  say  that  its  color,  its  size,  its  weight,  and  all  its  other 
innumerable  properties,  is  the  same  as  the  color,  size,  weight,  and  other 
properties  which  I  know  in  other  objects.  Wherever  I  turn,  and  what- 
ever object  I  look  at,  I  cannot  get  rid  of  the  fundamental  relations  of 
sameness  and  difference,  and  consequently  the  name  of  these  simple 
relations  must  be  much  more  profoundly  organized  than  the  names  of 
things. 

In  dissolution  of  the  impressive  faculty  of  speech,  therefore,  the 
names  of  things  disappear  first  and  of  the  simple  relations  last.  Now 
of  all  words  the  individual  names  are  the  least  organized,  and  it  is 
within  the  experience  of  every  one  how  very  easy  it  is  to  forget  the 
names  of  one's  friends,  while  such  simple  predicates  as  is,  may,  and  shall, 
or  being,  go,  run,  and  know ;  adverbs  like  here,  there,  now,  before, 
and  after;  adjectives  like  good  and  bad,  and  hard  and  soft,  are  un- 
doubtedly much  more  frequently  repeated  in  speech  than  the  names  of 
persons  and  things,  and  the  former  are,  therefore,  more  likely  to  be 
preserved  than  the  latter  in  cases  of  dissolution  of  the  impressive  faculty 
of  speech.  In  those  cases  of  aphasia  in  which  the  names  of  persons 
and  things  are  almost  entirely  lost,  let  it  not  be  thought  that  the  other 
parts  of  speech  have  suffered  no  damage.  The  patient  whose  case  I 
have  already  mentioned,  who  named  every  object  presented  to  him, 
including  his  own  fingers,  "  public  house,"  "glass  of  beer,"  or  "half- 
penny," was  accustomed  to  describe  his  previous  occupation  in  the 
following  terms  :  "  When  gentlemen  got  into  trouble  I  brought  an  action 
against  them  and  they  were  all  right  then."  He  was  a  messenger  in 
the  bankruptcy  court  and  had  to  serve  processes  on  defaulting  debtors. 
He  must,  therefore,  have  been  very  familiar  with  such  words  as  "  to 
liquidate,"  and  with  such  phrases  as  "  to  compound  with  one's  creditors," 
but  he  now  never  uses  such  complex  words  and  does  not  give  any  evi- 
dence that  he  understands  them  when  uttered  in  his  presence.  It  must, 
therefore,  be  presumed  that  in  him  all  other  parts  of  speech  as  well  as 
the  nouns  have  suffered  damage,  inasmuch  as  he  is  only  able  to  make 
use  of  those  words  and  phrases  which  express  the  simplest  relations, 
and  qualities,  and  the  events  most  frequently  repeated  in  his  experience. 
In  dissolution  of  the  nervous  mechanism  of  the  impressive  faculty  of 
speech  the  names  of  persons  and  things  disappear  first  because  they  are 
the  least  organized.  The  facility  with  which  proper  nouns  are  lost  has 
been  experienced  by  most  of  us  in  the  readiness  with  which  we  forget 
the  names  of  our  most  intimate  friends  when  the  brain  is  fatigued  by 


650  APHASIA. 

overwork  or  loss  of  sleep.  Most  educated  men  have  also  experienced 
the  strong  tendency  which  the  technical  language  of  a  newly  acquired 
science  has  to  fade  from  the  memory.  But  although  the  loss  of  the 
nouns  is  the  most  marked  feature  of  sensory  aphasia  it  must  be  ad- 
mitted that  this  disability  is  accompanied  by  the  loss  of  all  words  which 
express  complex  relations  and  qualities,  and  the  Avords  which  remain  to 
the  last  are  those  which  express  the  relations  and  qualities  which  have 
been  most  frequently  repeated  in  the  experience  of  the  race,  and  the 
events  which  have  been  most  frequently  repeated  in  the  experience  of 
the  individual.  It  must,  however,  be  remembered  that  frequency  of 
repetition  is  only  one  factor  in  producing  degrees  of  organization  in 
speech.  The  strength  of  the  impression  Avhich  formed  the  association 
between  the  word  and  the  thing  signified  by  it,  as  well  as  various  other 
circumstances,  must  be  taken  into  account.  "  Burnt  children  dread  the 
fire,"  and  doubtless  the  word  fire  becomes  deeply  fixed  in  the  organiza- 
tion from  a  very  limited  experience  of  its  action.  But  as  it  is  impossible 
to  pursue  the  subject  further  in  this  ])lace,  the  student  must  be  left  to 
think  it  out  for  himself.  That  word-deafness,  and  word-blindness  are 
examples  of  partial  anaesthesia  is  well  illustrated  by  recorded  cases  in 
which  a  person,  while  suffering  from  one  of  these  affections,  suddenly 
becomes  completely  deaf  or  blind  without  having  any  local  disease  in 
the  ear  or  eye,  and  at  the  autopsy  a  spot  of  softening  is  found  symmetri- 
cally pkced  in  each  hemisphere  of  the  brain  on  a  level  with  the  first 
and  second  temporo-sphenoidal  convolutions,  or  with  the  angular  gyn. 


CHAPTEE    XIX. 

DISEASES  OF  THE  MEMBRANES  OF  THE  BRAIN. 

I.  DISEASES    OF   THE    DURA   MATER. 

Inflammation  of  the  dura  mater  may  be  divided  into  (I.)  external, 
and  (II.)  internal  pachymeningitis. 

(I.)  External  Pachymeningitis. 

Etiology. — The  chief  causes  of  external  pachymeningitis  are  injuries 
which  detach  the  dura  mater  from  the  skull  and  give  rise  to  hemorrhage 
between  the  membrane  and  bones ;  perforating  injuries  of  the  skull : 
and  extension  of  inflammation  from  neio-hborinof  tissues,  as  from  the 
temporal  bone  in  caries  of  the  petrous  portion.  The  external  layer  of 
the  dura  mater  is  .subject  to  chronic  thickening  in  old  age. 

ST/inptoms. — In  traumatic  external  pachymeningitis  the  patient  may 
recover  from  the  immediate  effects  of  the  injury,  but  at  the  end  of  two 
or  three  weeks  he  suffers  from  pain  in  the  head  and  is  feverish,  and 
should  there  be  an  external  w^ound  it  assumes  an  unhealthy  aspect.  If 
the  inflammation  spread  further  the  headache  increases  in  intensity,  and 
the  patient  suffers  from  vertigo,  nausea,  and  vomiting,  while  mono- 
spasms, or  unilateral  convulsions  may  occur  if  the  motor  area  of  the 
cortex  is  affected.  As  the  inflammatory  process  extends  inwards  through 
the  pia  mater  to  the  cortex  the  previously  convulsed  limbs  become  para- 
lyzed, delirium  supervenes,  and  the  patient  soon  dies  in  coma. 

When  an  abscess  forms  between  the  bones  of  the  skull  and  the  dura 
mater  the  symptoms  may  be  those  of  gradual  cerebral  compression. 
In  the  pachymeningitis  of  old  age  the  symptoms  consist  of  a  persistent 
dull  headache,  and  in  many  cases  the  presence  of  the  disease  is  only 
discovered  post  mortem. 

(II.)  Internal  Hemorrhagic  Pachymeningitis  (Hematoma  of 
the  Dura  Mater). 

Etiology. — Hsematoma  of  the  cerebral  dura  mater  is  generally  met 
with  in  old  age,  and  is  either  caused  by  internal  injury,  or  results  from 


652      DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

cachectic  diseases  like  scorbutus,  chronic  alcoholism,  general  paralysis, 
and  senile  atrophy  of  the  brain. 

Symptoms. — The  symptoms  are  variable,  but  the  most  constant  is  a 
dull  headache,  which  is  generally  diffused,  but  may  be  more  pronounced 
on  one  side  than  the  other.  The  motor  disturbances  consist  of  unilat- 
eral or  bilateral  muscular  twitchings,  which  are  followed  by  a  persistent 
rigidity.  In  other  cases  paresis,  first  of  the  one  and  then  of  the  other 
extremity  of  the  same  side  occurs,  which  gradually  increases  until  a 
decided  hemiplegia  is  established.  In  some  cases  the  paralysis  extends 
to  the  other  side,  showing  either  that  the  inflammatory  action  has 
spread  to  the  other  side  or  that  a  fresh  hemorrhage  has  occurred,  form- 
ing a  new  focus  of  disease.  The  gait  is  often  uncertain,  and  the  patient 
experiences  difficulty  in  Avriting  and  speaking,  while  a  conjugate  devia- 
tion of  the  eyeballs  towards  the  side  of  the  lesion  is  not  infre(juently 
present.  Patients  sometimes  complain  of  formication  and  numbness  of 
the  paralyzed  side,  but  impairment  of  sensation  in  the  absence  of  paral- 
ysis never  occurs. 

Psychical  disturbances  are  sometimes  present  as  part  of  the  primary 
disease,  as  when  hematoma  occurs  in  general  paralysis,  but  at  other 
times  they  result  directly  from  the  luematoma.  These  disorders  con- 
sist at  first  of  great  mental  irritability,  abnormal  sensitiveness  to  light, 
and  ringing  in  the  ears,  but  as  the  disease  advances  the  signs  of  in- 
creased irritability  give  place  to  those  of  a  gradual  compression.  In 
other  cases  drowsiness  is  the  chief  psychical  symptom  observed,  and 
when  it  is  present  in  old  people  in  conjunction  with  chronic  headache 
and  contracted  or  dilated  j)upils,  luematoma  should  be  suspected.  The 
pupils  are  contracted  and  unirritable  to  liglit  during  the  irritative  stage 
of  the  disease,  but  dilatation  predominates  when  the  symptoms  of 
compression  supervene.  In  most  cases  the  pulse  is  slow  during  the 
early  stages  of  the  disease,  but  becomes  frequent  and  irregular  before 
death.  The  course  of  the  disease  is  very  variable.  It  usually  begins 
witli  more  or  less  acute  symptoms,  which  are  followed  by  an  interval  of 
comparative  health;  after  a  time  a  fresh  acute  attack  occurs,  which  may 
cause  death  or  is  followed  by  another  interval.  The  majority  of  cases 
terminate  fatally,  although  it  is  not  impossible  that  partial  recovery 
may  occasionally  take  place. 


DISEASES    OF    THE    PIA    MATER.  653 

II.  DISEASES  OF  THE  PIA  MATER. 

(I.)  TuBERCUi«vE  Meningitis  (Acute  Hydrocephalus). 

Etiology. — Most  of  those  ■who  suffer  from  tubercular  meningitis 
belong  to  families  in  which  the  tubercular  diathesis  is  distinctly  marked. 
The  largest  proportion  of  cases  of  tubercular  meningitis  should  occur 
in  croAvded  populations  and  large  cities,  and  amongst  the  poorest  and 
most  neglected  part  of  the  population.  Season  does  not  appear  to 
exert  any  influence  in  the  production  of  the  disease.  Tubercular  men- 
ingitis may  set  in  at  any  age,  but  it  is  much  more  frequent  between 
the  ages  of  two  and  seven  years.  The  numbers  diminish  from  the 
seventh  to  the  tenth,  and  in  still  greater  proportion  from  the  tenth  to 
the  fifteenth  year.  In  adults  it  is  most  common  between  the  ages  of 
tAN'enty  and  forty,  and  occurs  very  exceptionally  after  the  forty-fifth 
year.  The  male  sex  appears  to  be  more  frequently  affected  than  the 
female.  In  adults  the  proportion  is  51.5  men  to  48.5  women,  and  the 
proportion  of  males  affected  in  children  is  still  greater. 

Symptoms. — Premonitory  s}'mptoms  manifest  themselves  for  a  varia- 
ble period  of  weeks  or  months  before  the  development  of  the  distinctive 
phenomena  of  tubercular  meningitis,  the  most  constant  of  these  being 
a  gradual  loss  of  flesh  without  perceptible  cause,  which  is  more  noticea- 
ble in  the  trunk  and  limbs  than  in  the  face,  loss  of  appetite,  constipa- 
tion or  diarrha^a,  and  an  undefined  feeling  of  illness  and  weariness. 

As  the  invasion  approaches  the  patient,  Avhen  a  child,  loses  his 
vivacity,  becomes  sad,  fretful,  taciturn,  irritable,  and  Avants  to  be  left 
alone,  and  in  the  midst  of  play  leaves  his  companions  in  order  to  give 
vent  to  his  distress  in  tears.  He  sleeps  with  eyes  half  open,  and  grinds 
his  teeth,  while  his  sleep  is  disturbed  by  muscular  twitches  and  horri- 
ble dreams,  so  that  he  frequently  starts  and  cries  out. 

On  awakening  he  complains  of  headache,  and  after  a  time  a  slight 
febrile  accession  is  observed  towards  evening  without  obvious  cause. 

In  some  cases  the  brain  symptoms  make  their  appearance  without 
any  warning,  and  the  first  symptoms  Avhich  indicate  an  affection  of  the 
pia  mater  may  be  violent  headache,  vomiting,  or  facial  paralysis,  fol- 
lowed quickly  by  unconsciousness. 

The  disease  itself  presents  [a)  an  initial  period  in  which  symptoms  may 
be  referred  to  excitation  of  the  cortex;  {h)  a  period  in  which  symptoms 
caused  by  excitation  are  mixed  with  those  due  to  progressive  pressure 
caused  by  effusion  and  to  lesions  at  the  base  of  the  brain ;  and  {c)  a 


651-      DISEASES    OF    THE    MEMBRANES    OF    THE    BKAIN. 

final  period  in  -which  symptoms  due  to  pressure  caused  by  the  ventricu- 
h\r  effusion  greatly  predominate. 

{a)  The  Period  of  Invasion. — In  some  cases  the  invasion  is  ushered 
in  by  a  chill,  accompanied  by  a  rapid  rise  of  temperature,  while  in 
others  there  are  distinct  shiverings,  violent  headache,  and  attacks  of 
giddiness.  Vomiting  is,  however,  the  most  common  special  symptom 
of  the  period  of  invasion.  It  varies  greatly  in  frequency,  but  as  a 
rule  occurs  only  twice  in  twenty-four  hours  during  the  first  two  or 
three  days  of  the  disease.  In  some  few  cases,  however,  the  child 
vomits  incessantly,  Avhether  food  is  taken  or  not,  but  when  once  the 
tendency  to  vomit  has  ceased  for  twenty-four  hours,  it  does  not  ordi- 
narily recur.  Constipation  is  present,  as  a  rule,  throughout  the  whole 
course  of  the  disease.  Although  there  are  occasional  exceptions,  the  con- 
stipation is  not  often  obstinate,  and  it  is  generally  easy  to  procure 
action  of  the  bowels  by  ordinary  means. 

Headache,  of  a  dull,  heavy,  or  lancinating  character,  is  usually  an 
urgent  symptom  while  consciousness  is  retained,  and  its  temporary 
exacerbations  are  made  known  by  moaning  or  shrieks,  while  even  after 
unconsciousness  has  set  in  the  patient  puts  his  hand  to  his  head,  wrinkles 
his  forehead,  and  distorts  his  face  as  if  from  pain.  Vertigo  is  always 
present.  Patients  feel  as  if  they  were  falling  in  bed,  or  as  if  surround- 
ing objects  were  revolving  around  them,  and  the  gait  is  often  reeling 
and  unsteady,  but  the  rapid  development  of  severe  symptoms  soon  pre- 
vents all  attempts  at  station  and  locomotion. 

The  motor  disturbances  consist  of  spasmodic  movements  in  the  form 
of  partial  convulsions,  giving  rise  to  tremor  and  conjugate  deviation  of 
the  eyeballs,  with  rotation  of  the  head  and  neck,  strong  convergent 
and  divergent  S({uints,  grinning  contortions  of  the  muscles  of  the  face, 
and  grinding  of  the  teeth.  It  is  probable  that  the  hydrocephalic  cry, 
which  so  commonly  occurs  during  this  period  of  the  disease,  Avhich  Trous- 
seau says  is  '"single  and  loud,  like  the  cry  of  a  person  frightened  by 
some  sudden  danger,"  is  due  to  spasmodic  action  of  the  respiratory  and 
laryngeal  muscles,  and  is  quite  independent  of  consciousness.  The 
muscles  of  the  neck  and  back  are  often  persistently  contracted,  and 
the  abdomen  is  retracted,  owing  to  spasm  of  its  muscles,  so  that  it 
presents  a  characteristic  boat-shaped  depression.  In  children  epilepti- 
form convulsions  are  not  uncommon,  but  they  are  rare  in  adults,  and 
towards  the  end  of  this  stage  slight  paralysis  of  the  ocular  and  facial 
muscles  may  be  present,  as  declared  by  inequality  of  the  pupils,  ptosis, 
strabismus,  or  slight  facial  paralysis. 

The  sensory  disturbances  are  often  obscured  by  loss  of  consciousness, 
but  at  times  a  general  or  partial  hyperpesthesia  of  the  surface  of  the 


DISEASES    OF    THE    PI  A    MATER.  655 

body  may  be  observed  at  the  beginning  of  the  disease,  while  general  or 
partial  anaesthesia  is  not  infrequent  at  an  advanced  period  of  the  dis- 
ease, and  has  occasionally  been  observed  as  a  premonitory  symptom. 
Intolerance  of  sound  and  light  is  a  prominent  symptom;  the  child  is 
impatient  of  the  slightest  noise,  and  avoids  the  light  by  lying  with  the 
face  buried  in  the  pillow  or  turned  towards  the  wall,  with  the  knees 
drawn  up  towards  the  abdomen,  and  the  eyelids  firmly  closed. 

Psychical  disturbances  are  not  always  present  in  the  early  period  of 
the  affection.  The  patient  cannot,  however,  form  consecutive  trains  of 
ideas,  and  children  soon  become  somnolent,  lie  with  their  eyes  closed, 
and  reply  to  questions  curtly  or  merely  by  a  nod.  When  raised  up, 
they  complain  much,  knit  their  brows,  throw  back  their  heads,  and  slip 
down  in  bed ;  they  cannot  bear  the  slightest  disturbance,  and  will  clench 
their  teeth  against  food.  Delirium  is  of  frequent  occurrence  when  the 
patient  is  half  asleep;  and,  in  the  case  of  children,  the  hydrocephalic 
cry  is  not  infrequently  heard  at  this  time,  being  accompanied  by  start- 
ing up  in  terror.  At  other  times  the  patient  may  spring  from  bed,  or 
make  defensive  movements  in  consequence  of  hallucinations  of  sight 
and  hearing.  The  somnolence  soon  increases,  tbe  eyes  stare  without 
expression  into  vacancy,  and  the  patient  ceases  to  speak  to  his  atten- 
dants, but  he  talks  senselessly  with  himself,  or  laughs,  sings,  whistles, 
or  shouts,  and  performs  meaningless  movements,  such  as  plucking  at 
imaginary  objects,  picking  the  bedclothes,  blowing,  spitting,  and  grim- 
acing. After  a  time  these  disturbances  cease,  and  the  mental  faculties 
may  again  become  completely  or  partially  clear,  but  after  a  longer  cr 
shorter  period,  new  and  more  profound  disturbances  supervene,  which 
increase  until  the  fatal  termination. 

Disorders  of  vision  are  seldom  absent  in  this  stage  so  long  as  the 
patient  is  tolerably  conscious,  and  an  ophthalmoscope  may  reveal  the 
presence  of  double  optic  neuritis,  or  tubercles  of  the  choroid. 

The  pulse  is,  as  a  rule,  slow  and  full  during  the  early  stage  of  the 
affection,  but  it  is  subject  to  rapid  variations  during  muscular  exertion 
of  every  kind  and  psychical  excitement,  especially  in  the  case  of  children. 
The  temperature  is  very  inconstant,  and  does  not  conform  to  any  type. 
The  skin  is  usually  dry,  and  even  in  those  cases  where  the  tubercular 
meningitis  is  associated  with  phthisis,  the  sweats  of  the  latter  disease 
usually  cease  when  the  meningitis  manifests  itself.  It  has  also  been 
observed  that  the  cough,  dyspnoea,  and  expectoration  of  phthisis  cease, 
and  in  the  case  of  intestinal  tuberculosis  the  diarrhoea  is  arrested.  The 
injection  of  the  face  and  conjunctiva  varies  frequently  without  obvious 
cause;  lividity  of  the  face  belongs  to  a  later  period,  or  is  dependent  on 
lung  complications. 


656       DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

The  average  duration  of  the  first  stage  is  about  eight  days,  but  it 
varies  from  two  days  to  two  or  three  weeks,  and  is  not  unfrequently 
followed  by  a  remission  which  leads  the  friends  of  the  patient  to  hope 
for  a  favorable  termination. 

(b)  The  second  stage  is  now  ushered  in  with  the  evidences  of  loss  of 
functional  activity.  The  signs  of  excitement  become  less  frequent,  and 
somnolence  and  mental  torpor  more  prominent,  but  even  in  the  midst 
of  sopor  adults  give  evidence  of  suffering  from  severe  headache  by 
groans  and  gestures,  while  in  children  the  hydrocephalic  cry  is  frequently 
heard  at  this  stage. 

The  presence  of  muscular  spasms  is  declared  by  combined  movements 
of  the  eyeballs  or  nystagmus,  iiie(iuality  of  the  pupils,  winking  and 
facial  contortions,  and  grinding  of  the  teeth  with  munching  movements 
of  the  jaws,  Avhile  in  some  cases  one  or  more  of  the  limbs  are  agitated 
by  tremors  or  choreic  movements,  and  in  rare  cases  the  muscles  of  the 
trunk  and  limbs  are  maintained  in  a  state  of  cataleptic  rigidity. 

The  stiffness  of  the  muscles  of  the  nape  of  the  neck  becomes  more 
intense,  so  that  the  head  is  drawn  back  and  thrust  into  the  pillow.  The 
rigidity  may  also  extend  to  the  muscles  of  the  trunk,  and  the  body  is 
maintained  in  a  condition  of  tetanic  rigidity,  the  opisthotonos  either 
appearing  in  paroxysms  and  lasting  only  a  few  minutes  at  a  time,  or 
remaining  continuous  until  death.  Paralyses  of  various  extent  and 
distribution  now  make  their  appearance.  Paralysis  of  the  oculo-motor 
nerve  is  common,  and  gives  rise  to  divergent  squint,  ptosis,  and  dilata- 
tion, with  fixity  of  one  or  both  pupils.  The  trochlear  nerve  may  be 
paralyzed  along  with  the  third,  but  is  never  affected  alone.  Paralysifs 
of  the  abducens  may,  however,  occur  as  a  separate  affection.  The 
paralytic  form  of  conjugate  deviation  of  the  eyes  and  rotation  of  the 
head  and  neck  may  appear  at  this  ])eriod  of  the  disease,  and  decided 
paralysis  of  one  side  of  the  face  is  often  present,  while  the  tongue  is 
drawn  towards  the  paralyzed  side  on  protrusion.  It  is  not  uncommon 
for  aphasia  to  occur,  especially  in  adults,  in  this  stage  of  the  disease. 
The  disorder  of  speech  may  either  be  a  sensory  or  a  motor  aphasia,  or 
a  sensory  aphasia  may  appear  first,  then  there  is  a  ra])id  im])rovement, 
but  soon  a  motor  aphasia  is  superadded  and  in  a  few  days  the  patient 
dies  comatose  after  suffering  probably  from  severe  general  convulsions. 

Hemiplegia  and  hemiparesis  are  rare,  but  monoplegias  are  frequent. 
At  times  one  arm  or  one  leg  is  paretic  or  completely  paralyzed  ;  while 
occasionally  the  paralysis  assumes  the  paraplegic  form,  or  a  considerable 
diminution  of  strength  may  occur  in  all  four  extremities. 

The  sensory  disorders  consist  of  partial  anaesthesia  which  may  be 
limited  to  one  or  other  extremity  or  to  the  side  of  the  face,  but  as  the 


DISEASES    OF    THE     PIA    MATER.  657 

disease  progresses  the  anaesthesia  becomes  more  profound,  and  distributed 
over  the  whole  body.  The  optic  disks  are  markedly  swollen  in  this 
stage,  and  retinal  hemorrhages  are  a  frequent  complication. 

Vomiting  is  an  occasional  symptom  of  this  stage,  the  constipation 
continues,  and  the  urine  is  generally  passed  in  bed  or  there  is  complete 
retention.  The  pulse  becomes  less  frequent,  and  may  sink  to  sixty  or 
still  lower,  and  is  at  the  same  time  fuller ;  but  the  slightest  excitement 
may  raise  the  number  of  beats  to  more  than  one  hundred  per  minute, 
and  it  is  apt  to  become  irregular.  The  temperature  varies,  and  although 
it  usually  conforms  to  the  remittent  type  in  children  which  is  so  charac- 
teristic of  tuberculosis  of  other  organs,  yet  it  should  be  remembered  that 
in  adults  it  may  remain  almost  completely  normal  throughout  this  stage 
of  the  disease. 

The  respiration  is  sometimes  normal,  at  other  times  irregular,  and  it 
occasionally  assumes  the  character  of  the  Cheyne-Stokes  respiration. 
Neuro-paralytic  oedema  of  the  lungs  is  liable  to  occur  at  this  period  of 
the  disease.  This  period  may  last  about  a  week,  and  then  the  third 
stage  of  the  disease  is  ushered  in  by  the  appearance  of  persistent  coma. 

{c)  The  Third  Stage. — The  patient  is  now  completely  insensible  to 
most  external  excitants,  and  most  reflex  actions  are  extinguished,  al- 
though he  may  still  respond  to  a  loud  voice  close  to  the  ear. 

Isolated  paralyses  are  not  now  so  readily  observed,  inasmuch  as  there 
is  general  relaxation  of  the  whole  muscular  system,  but  rigidity  of  the 
masticatory  muscles  and  of  the  muscles  of  the  back  and  extremities  is 
sometimes  still  present.  Convulsions  are  rare  in  adults  ;  but  in  children 
partial  convulsive  spasms  may  occur,  and  immediately  before  death  the 
patient  may  be  seized  with  general  convulsions.  The  electric  excit- 
ability of  the  muscles  to  both  constant  and  induction  currents  is  normal. 
Every  form  of  sensibility  is  now  completely  abolished.  The  pupils  are 
dilated  and  fixed,  the  upper  lids  fall  inert  and  paralyzed  over  the  eye- 
balls, and  an  ophthalmoscopic  examination  reveals  signs  of  marked 
oedema  of  the  optic  disks.  The  pulse  during  this  period  becomes  more 
and  more  frequent  and  may  be  irregular,  and  in  the  case  of  children 
the  pulsations  of  the  fontanelles  become  weaker  and  weaker,  and  may 
disappear  before  death. 

The  respiration  is  irregular,  and  at  times  so  superficial  and  feeble 
that  it  may  escape  observation,  while  at  other  times  it  is  forced  and  deep. 
Kapid  emaciation  occurs,  especially  in  the  case  of  children  ;  the  skin 
is  generally  dry  and  rough,  and  it  may  become  slightly  livid  with  the 
decreasing  force  of  the  heart ;  and  occasionally  a  bedsore  a})pears.  The 
temperature  during  this  period  varies  greatly.  In  some  cases  it  is  below 
normal,  and  immediately  before  death  may  sink  as  low  as  95°  F.  or 

42 


658       DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

even  93°  F.  In  another  series  of  cases  a  state  of  moderate  fever  con- 
tinues up  to  the  time  of  death  ;  while  in  a  third  group  the  fever  greatly 
increases  before  death,  and  may  even  continue  to  increase  for  some  time 
afterwards. 

The  urine  is  generally  scanty  with  high  specific  gravity  ;  its  quantity 
may  be  increased  or  normal ;  the  proportion  of  chlorides  varies  greatly  ; 
and  the  phosphates  are  said  to  be  increased.  A  small  quantity  of 
albumen  is  frequently  present,  but  sugar  is  rare.  The  duration  of 
the  paralytic  stage  is  generally  three  or  four  days,  and  seldom  reaches 
a  week. 

The  course  of  tubercular  meningitis  is  very  variable.  In  some  cases 
it  runs  a  rapid  course  and  terminates  fatally  in  five  or  six  days.  In 
other  cases  the  disease  is  very  protracted ;  the  invasion  is  slow  and 
insidious,  and  the  disease  may  last  from  thirty  to  fifty  or  even  sixty  days. 


Chronic  Hydrocephalus. 

The  etiology  of  chronic  hydrocephalus  is  not  well  known  ;  but  hered- 
itary predis})Osition  appears  to  exert  some  influence  in  its  production, 
for  more  than  one  child  may  be  affected  in  the  same  family.  Congenital 
syphilis  is  probalily  the  most  important  predisposing  cause,  and  it  is 
possible  that  too  much  importance  lias  been  attributed  to  rickets  in  its 
production.  The  disease  is  always  congenital  or  acquired  soon  after 
birth,  except  when  it  results  from  intracranial  tumors  or  from  occlusion 
of  one  or  more  of  the  lateral  sinuses.  Of  the  exciting  causes  little  is 
known.  Chronic  hydrocephalus  is  sometimes  preceded  by  an  attack 
resembling  acute  hydrocephalus. 

Symptoms. — In  congenital  hydrocephalus  cerebral  symptoms,  such 
as  daily  recurring  convulsions,  strabismus,  or  rolling  of  the  eyeballs, 
are  apparent  from  the  infant's  birth,  while  in  a  few  days  or  weeks  the 
head  is  observed  to  undergo  progressive  enlargement. 

Impairment  of  the  general  nutrition  is  one  of  the  first  symptoms; 
the  child  may  seem  eager  for  food  and  sucks  well,  yet  it  loses  flesh  and 
strength,  and  the  skin  hangs  in  loose  folds  on  its  attenuated  limbs. 
The  bowels  are  generally  constipated,  or  diarrhoea  may  alternate  with 
constipation,  and  the  evacuations  are  always  unhealthy.  The  child  is 
restless  and  may  be  drowsy  during  the  day,  but  wakeful  and  fretful 
during  the  night.  The  fontanelles  and  sutures  are  now  unusually  open, 
the  anterior  fontanelle  is  tense  and  pulsates  strongly,  and  the  child  is 
subject  to  paroxysms  of  restlessness,  during  which  there  is  increased 
heat  of  the  head. 


DISEASES    OF    THE    PIA    MATER.  659 

The  sutures  become  gradually  Avicler  with  the  increase  of  effusion, 
the  fontanelles  increase  in  size,  the  head  assumes  a  globular  form,  and 
the  physiognomy  of  the  child  soon  acquires  the  characteristic  features 
of  chronic  hydrocephalus.  As  the  fluid  accumulates  within  the  cranium 
it  presses  equally  in  all  directions,  and  the  cavity  of  the  skull  must 
enlarge  in  the  direction  of  least  resistance.  The  greatest  increase  in 
the  size  of  the  head  is  effected  chiefly  by  enlargement  of  the  anterior 
fontanelle  and  by  widening  of  the  sagittal  suture,  these  being  the  points 
which  are  the  last  to  be  ossified,  and  at  which  the  bones  of  the  skull 
are  less  firmly  fixed.  The  frontal  bones  are  consequently  pushed  for- 
wards, rendering  the  forehead  round  and  prominent,  the  parietal  bones 
are  pressed  backwards  and  outwards,  and  the  occipital  bone  downwards 
and  backwards,  sometimes  even  so  far  that  it  assumes  an  almost  hori- 
zontal position.  The  head  is,  as  a  rule,  globular  and  flat  at  the  top, 
although  it  occasionally  assumes  a  conical  form.  Its  size  varies,  and  it 
has  been  known  to  measure  two  or  even  three  feet  in  circumference.  The 
orbital  plates  of  the  frontal  bones  are  pushed  from  the  horizontal  to  an 
oblique,  or  it  may  be  almost  vertical  position,  and  thus  encroach  upon 
the  cavities  of  the  orbits.  The  eyeballs  are  consequently  pressed  for- 
wards and  rendered  prominent ;  they  are  at  the  same  time  rotated  down- 
wards, so  that  the  sclerotic  coat  appears  below  the  upper  lids,  while  the 
pupils  are  half  hidden  beneath  the  lower  lids.  On  placing  the  hand 
over  the  open  fontanelles  and  sutures  they  are  felt  tense  and  fluctuating. 
The  hair  grows  scantily  over  the  head,  and  the  skin  is  tense  and  shining, 
differing  in  this  respect  from  the  wrinkled  condition  of  that  of  the  rest  of 
the  body ;  distended  veins  ramify  over  the  scalp ;  and  the  enlarged  head 
contrasts  strikingly  with  the  small  infantile  face.  The  child  has  a  dull 
and  stupid  expression,  and  being  unable  to  hold  his  head  up  he  is  obliged 
to  remain  in  the  recumbent  posture  or  to  assume  a  half-sitting  position, 
while  his  head  is  supported  with  his  hands  or  propped  up  with  pillows. 
The  most  usual  cerebral  symptoms  which  appear  during  the  progress  of 
the  case  are  convulsions  ;  attacks  of  laryngismus  stridulus ;  paralyses 
with  contractures  of  varying  distribution  ;  rolling  of  the  eyeballs ;  and 
amblyopia  progressing  to  amaurosis.  Hearing,  as  a  rule,  remains  un- 
affected until  near  the  fatal  termination.  Chronic  hydrocephalus  lasts 
usually  from  one  to  two  years,  but  in  exceptional  cases  the  patient  has 
been  known  to  live  to  middle  or  even  old  age.  The  disease  is  almost 
always  fatal,  death  being  caused  by  laryngismus  stridulus,  general  con- 
vulsions, or  some  intercurrent  disease. 


660      DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

(II.)  Meningitis  of  the  Convexity  of  the  Brain. 

Etiology. — Simple  primary  meningitis  of  the  convexity  of  the  brain 
is  a  rare  affection.  It  may  occur  at  all  ages,  but  chiefly  attacks  infants 
under  two  years  of  age,  when  it  is  named  leptomeningitis  infantium. 
It  occurs  with  decreasing  frecjuency  from  this  age  to  puberty,  when  it 
becomes  more  frequent,  but  it  is  only  very  rarely  met  with  in  advanced 
ao-e.  In  adults  men  are  more  frequently  attacked  than  women.  The 
exciting  causes  of  the  disease  are  not  well  known. 

Secondary  meningitis  of  the  convexity  may  be  produced  by  inflam- 
mation of  the  bones  of  the  skull,  the  usual  causes  of  the  latter  being 
external  injury,  scrofula,  and  syphilis.  Gummata  may  also  give  rise 
to  this  inflammation.  Otorrhtiea,  especially  when  complicated  by  caries 
of  the  temporal  bone,  is  one  of  the  most  frequent  causes  of  purulent 
menino-itis,  and  the  affection  may  result  from  puriform  softening  of  a 
thrombus  in  one  of  the  sinuses,  erysipelas  of  the  head  leading  to  osteo- 
phlebitis of  the  bones  of  the  skull,  carbuncles  of  the  face  and  neck, 
suppuration  of  the  eyeball,  and  all  intracranial  diseases  like  tumors, 
abscesses,  or  necrotic  softening. 

Symptoms  of  Primary  Meningitis  of  the  Convexity. — The  course  of 
acute  meningitis  may  be  divided  into  three  stages:  (1)  The  period  of 
excitement,  (2)  the  period  of  transition,  and  (3)  the  stage  of  collapse. 

(1)  The  Period  of  Excitement. — Obscure  premonitory  sym])toms 
are  sometimes  observed,  consisting  usually  of  a  feeling  of  heaviness  in 
the  head  along  with  paroxysms  of  violent  cephalalgia,  sleeplessness, 
irritability  of  temper,  and  general  malaise.  As  a  rule,  however,  the 
disease  begins  suddenly  by  a  well-marked  rigor,  intense  headache, 
vomiting,  fever,  and  delirium,  while  in  children  it  is  ushered  in  by  an 
attack  of  general  convulsions. 

The  headache  may  be  diffused  or  referred  to  the  forehead,  temples, 
vertex,  or  occiput;  it  is  intensified  by  light  and  sound,  and  by  all 
movements  of  the  head.  The  patient  consequently  shuns  the  light, 
and  holds  his  head  between  his  hands,  in  order  to  prevent  it  from 
moving.  The  headache  is  continuous,  but  is  marked  by  exacerbations 
of  intense  severity,  during  which  the  patient,  especially  if  a  child,  may 
utter  a  loud  and  piercing  cry. 

Vomiting  is  a  very  constant  symptom  of  meningitis,  and  is,  like  the 
vomiting  symptomatic  of  other  cerebral  diseases,  unattended  by  nausea, 
and  epigastric  pain  or  tenderness.  It  recurs  frequently  during  the  first 
forty-eight  hours,  and  may  then  cease  or  occur  at  intervals  throughout 
the  course  of  the  affection. 


DISEASES    OF    THE    PIA    MATER.  661 

The  motor  disturbances  in  this  stage  consist  of  strabismus,  slight 
twitching  of  the  muscles  of  the  face  and  limbs,  and  tonic  spasms  of  those 
of  the  neck  and  back,  Avhile  the  patient  staggers  if  he  attempts  to  walk. 
The  pupils  are  usually  contracted  or  unequal,  but  react  readily  to  lio-ht. 

The  sensory  disturbances  consist  of  buzzing  in  the  ears,  flashes 
before  the  eyes,  and  intolerance  of  light  and  sound.  Cutaneous  hyper- 
aesthesia  is  not  infrequently  present,  so  that  the  slightest  touch  on  the 
skin  may  cause  pain,  and  the  reflex  excitability  is  increased. 

The  psychical  disturbances  are  well  marked  from  the  first.  The 
patient  is  extremely  iri-itable,  and  fierce  delirium  is  apt  to  occur,  the 
patient  shouting  and  violently  struggling  with  his  attendants.  At 
other  times  he  is  morose,  and  buries  his  head  under  the  bedclothes, 
obstinately  refusing  to  answer  questions.  The  temperature  of  the 
body  is  elevated,  the  pulse  beats  from  one  hundred  and  twenty  to  one 
hundred  and  forty  or  more,  and  the  respirations  are  increased  to  thirty 
or  forty  in  the  minute.     . 

(2)  The  Period  of  Transition. — During  this  period  the  furious 
delirium  of  the  first  stage  becomes  quieter,  the  patient  lies  on  his  back, 
with  his  fingers  picking  at  the  bedclothes  or  catching  imaginary  flies  in 
the  air. 

The  motor  symptoms  of  this  period  consist  of  strabismus,  conjugate 
deviations  of  the  eyeballs,  with  rotation  of  the  head  and  neck,  twitch- 
ings  of  the  face;  grinding  of  the  teeth  and  trismus;  distortions  of  the 
tongue;  the  hydrocephalic  cry;  subsultus  and  tremor  of  the  hand; 
convulsive  movements  of  the  limbs,  and  retraction  of  the  head  and 
neck  with  opisthotonos. 

These  convulsive  symptoms  are  followed  by  paralysis,  which  is  very 
variable  in  its  distribution,  some  groups  of  muscles  being  paralyzed 
while  others  continue  convulsed. 

The  sensory  disturbances  consist  of  dimness  of  vision  and  of  hearing, 
ending  in  blindness  and  deafness,  while  the  general  cutaneous  hyper- 
aesthesia  of  the  first  stage  is  replaced  by  anaesthesia.  The  bowels  ai'e 
constipated  throughout,  and  the  abdominal  walls  are  often  retracted  as 
in  tubercular  meningitis.  The  respirations  are  irregular,  the  pulse  fre- 
quent and  thready,  and  there  is  retention  of  urine. 

(3)  The  Stage  of  Collapse. — The  third  stage  of  the  afl'ection  now 
becomes  established,  the  convulsive  phenomena  give  place  everywhere 
to  paralysis,  and  the  patient  passes  into  a  profound  and  fatal  coma. 

Symptoms  of  Secondary  Meningitis. — The  symptoms  of  secondary 
meningitis  differ  considerably  according  to  the  cause  of  the  inflamma- 
tion, but,  inasmuch  as  inflammation  from  caries  of  the  petrous  bone  is 
the  most  usual  form  of  the  affection,  it  will  be  useful  to  describe  it  first. 


662      DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

The  affection  may  be  ushered  in  by  chilliness  or  a  distinct  rigor  and 
feverish  symptoms,  but  intense  headache,  either  continuous  or  marked 
by  remissions  and  exacerbations,  is  the  first  symptom  to  direct  attention 
to  the  brain.  The  headache  may  be  fixed  to  a  point  in  the  vicinity  of 
the  diseased  ear,  or  shoot  from  one  ear  to  another,  while  at  other  times 
it  is  diffused  over  the  whole  head.  If  the  local  affection  be  attended 
by  pain,  the  commencement  of  the  meningitis  is  marked  by  a  great 
increase  of  its  intensity,  and  the  onset  of  the  latter  may  sometimes  be 
completely  masked  by  an  increase  of  the  local  inflammation  in  the  ear. 
Attacks  of  dizziness  now  supervene,  accompanied  by  nausea  and  vomit- 
ing ;  the  patient  complains  of  noises  in  the  head,  general  painful  sensa- 
tions diffused  over  the  body,  and  obscuration  of  the  special  senses,  while 
he  often  becomes  actively  delirious. 

The  motor  symptoms  are  rigidity  of  the  muscles  of  the  nape  of  the 
neck,  convulsive  twitching  of  the  facial  muscles  on  the  affected  side, 
trismus,  grinding  of  the  teeth,  and  occasionally  .spasms  of  the  extremities. 

The  spasmodic  phenomena,  however,  soon  give  place  to  paralysis 
affecting  first  the  facial,  hypoglossal,  and  glosso-pharyngeal  nerves,  and 
should  the  inflammation  extend  forwards  along  the  base  of  the  skull, 
the  third,  fourtli,  sixth,  and  probably  the  fifth  nerves  on  the  same  side 
as  the  lesion.  The  state  of  the  pupils  is  variable,  and  liable  to  frequent 
changes  during  the  course  of  the  disease,  being  generally  contracted  or 
unequal  at  first,  and  dilated  and  fixed  wlien  effusion  has  taken  j)lace. 
Paralysis  of  the  extremities  is  rare,  but  the  patient  has  an  unsteady, 
staggering  gait. 

The  sensoty  disturbances  consist  of  marked  hyperaesthesia  of  the 
skin,  joints,  bones,  and  muscles,  so  that  every  movement  is  painful. 

Vomiting  generally  continues  throughout  the  whole  course  of  the 
disease,  the  bowels  are  constipated,  and  the  abdominal  muscles  are 
tender  to  the  touch  and  retracted.  The  temperature  in  acute  cases  is 
usually  high,  but  remits  in  the  morning,  although  it  remains  constantly 
high  in  some  cjises. 

The  pulse,  as  a  rule,  rises  and  falls  in  frequency  along  with  the  tem- 
perature, except  in  the  cases  where  symptoms  of  compression  of  the 
brain  occur  during  the  first  days  of  the  disease. 

The  urine  is  often  albuminous,  and  this  may  or  may  not  be  associated 
with  amyloid  disease  of  the  liver,  spleen,  and  kidneys. 

The  optic  disks  usually  present  the  same  ajipearances  as  those  observed 
in  tubercular  meningitis.  The  psychical  symptoms  are  very  variable, 
consisting  of  jactitation,  restlessness,  and  confusion  of  ideas,  especially 
towards  evening,  when  the  temperature  rises.  After  a  time  the  patient 
falls  into  a  somnolent  condition,  from  which  he  can  at  first  be  readilv 


DISEASES    OF    THE    PIA    MATER.  663 

roused  by  a  loud  question,  but  this  state  soon  gives  place  to  profound 
and  fatal  coma. 


(III.)  Simple  Meningitis  of  the  Base  of  the  Brain  (Basilar 

Meningitis). 

Etiology. — Inflammatory  processes  at  the  base  of  the  brain  are  caused 
by  fissures,  tumors,  abscesses  and  other  lesions  at  the  base  of  the  brain, 
but  the  form  to  be  described  at  present  arises  spontaneously,  and  occurs 
in  persons  from  sixteen  to  thirty  years  of  age. 

S'i/Diptoms. — When  primary  basilar  meningitis  is  diffused  and  general, 
the  affection  begins  by  languor,  mental  depression,  chilliness  or  even 
rigor,  thirst,  and  the  usual  symptoms  of  fever.  The  patient  complains 
of  intense  cephalalgia  and  giddiness,  and  these  are  followed  by  severe 
attacks  of  vomiting. 

Motor  disturbances  may  be  completely  absent  throughout  the  whole 
course  of  the  affection,  but  when  present  they  consist  of  spasmodic 
rigidity  of  the  muscles  of  the  back  of  the  neck,  with  retraction  of  the 
head,  and  rarely  of  rigidity  or  clonic  twitchings  of  certain  groups  of 
the  muscles  of  the  extremities.  The  patient  grinds  his  teeth  during 
sleep,  and  in  the  later  stages  of  the  affection  trismus  and  hiccough  have 
been  observed.  Paralysis  of  the  abducens  is  not  uncommon,  but  paral- 
ysis of  the  oculo-motor  nerve  is  rare.  Paresis  of  the  facial  or  hypo- 
glossal nerves  may  occur  temporarily  during  the  course  of  tlie  affection, 
and  subse(|uently  disappear,  but  complete  paralysis  of  them  has  not 
been  observed.  The  power  of  deglutition  may  be  impaired  during  the 
course  of  the  affection  and  be  afterwards  regained,  or  it  may  increase 
to  complete  dysphagia  before  death.  Paresis  of  the  extremities  is  occa- 
sionally observed,  but  never  complete  paralysis. 

The  sensory  disturbances  consist  of  cutaneous  hyper?esthesia,  espe- 
cially in  the  region  of  distribution  of  the  fifth  nerves,  ringing  in  the 
ears,  scintillations  before  the  eyes,  and  occasionally  hallucinations.  The 
psychical  disturbances  are  more  variable  than  in  any  other  form  of 
meningitis.  In  some  cases  the  mental  faculties  are  unaffected  through- 
out the  whole  course  of  the  disease,  while  in  others  they  are  early  in- 
volved. The  mental  symptoms  usually  consist  of  a  mild  delirium ;  but 
in  exceptional  cases  this  may  be  more  active,  the  patient  being  restless, 
quarrelsome,  capricious,  and  irascible.  Active  delirium  is  usually  tem- 
porary and  soon  gives  place  to  a  milder  form ;  the  patient  after  a  time 
becomes  somnolent,  but  may  be  temporarily  aroused  by  a  loud  (juestion 
addressed  to  him  ;  in  a  short  time  he  fails  into  a  state  of  complete  in- 


664      DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

sensibility,  during  which  the  urine  and  feces  are  passed  involuntarily. 
Vomiting  continues  to  distress  the  patient  throughout  the  course  of  the 
disease,  the  bowels  are  constipated,  but  the  abdomen  is  not  retracted  as 
in  tubercular  meningitis. 

The  temperature  may  rise  in  the  first  stage  as  high  as  104°  F.  in  the 
evening  and  approach  to  the  normal  in  the  morning,  but  in  the  later 
stages  the  temperature  remains  low,  being  sometimes  subnormal.  The 
pulse,  as  a  rule,  follows  the  temperature,  being  very  frequent  in  the 
initial  period,  and  sinking  in  the  course  of  the  disease  to  below  sixty 
beats  in  the  minute.  Towards  the  end  of  life  it  again  increases,  and 
becomes  very  frequent,  irregular,  and  intermittent ;  the  patient  is  covered 
with  bedsores,  much  emaciated,  and  dies  in  a  state  of  marasmus. 

The  chronic  forms  of  basilar  meningitis  may  give  rise  to  localized 
inflammatory  products  at  the  base  of  the  brain,  which  cause  symptoms 
scarcely  to  be  distinguished  from  those  of  tumors  occupying  the  same 
situation.  The  symptoms  are  variable  in  such  cases,  the  most  charac- 
teristic being  paralyses  of  the  various  cranial  nerves.  In  addition  to 
the  headache  and  dizziness,  there  are  anosmia,  amaurosis,  or  hemianopsia, 
ptosis,  paralysis  of  the  motor  nerves  of  the  eyeball,  sensory  disturbances 
in  the  region  of  distribution  of  the  fifth  nerve,  masticatory  paralysis, 
paresis  of  the  seventh  nerve,  and  occasionally  paresis  of  one  or  more  of 
the  extremities.  If  the  inflammation  extend  to  the  lower  end  of  the 
pons,  bulbar  paralysis,  dysphagia,  and  dyspnoea  may  be  present. 

(IV.)  Metastatic  Menixiutis. 

Metastatic  meningitis  comprises  certain  varieties  of  the  affection, 
which  occur  as  terminal  phenomena  in  the  course  of  acute  diseases. 

The  diseases  with  which  meningitis  is  most  fre(iuently  associated  are 
pneumonia,  ulcerative  endocarditis,  acute  rheumatism,  purulent  pleurisy, 
pericarditis,  diphtheria,  and  the  acute  exanthemata.  Although  chronic 
Bright's  disease  is  liable  to  be  complicated  by  inflammation  of  the  serous 
membranes,  meningitis  is  rare. 

Symptoms. — The  extent  and  intensity  of  the  inflammation  vary 
greatly  in  different  cases ;  in  some  there  is  little  or  no  effusion  into  the 
ventricles,  and  the  symptoms  of  compression  are  absent ;  the  inflamma- 
tion is  sometimes  limited  to  the  convexity,  and  at  other  times  extends 
to  the  base  and  upper  part  of  the  spinal  cord  ;  and  in  the  meningitis 
of  acute  febrile  diseases  the  symptoms  are  obscured  by  the  cerebral  dis- 
turbance usually  observed  in  all  grave  acute  affections. 


DISEASES    OF    THE    PIA     MATER.  665 

Varieties  of  Metastatic  Meningitis. 

Meningitis  ivith  Pneumonia. — Meningitis  may  appear  in  the  course 
of  pneumonia  from  the  third  to  the  eighth  day,  or  even  later.  The  most 
usual  symptoms  are  chilliness,  intense  headache,  rapidly  developed  and 
mild,  or  occasionally  furious  delirium,  a  fresh  accession  of  fever,  and 
hyperpyrexia  before  death.  The  delirium  gives  place  at  an  early  period 
to  somnolency,  ending  in  coma.  A  slight  degree  of  rigidity  and  pain 
in  the  neck  is  always  a  valuable  sign  of  meningitis,  and  vomiting  is  a 
frequent  occurrence.  The  pupils  are  generally  contracted  at  first,  and 
may  subsequently  become  unequal.  If  the  base  of  the  brain  be  affected, 
paralysis  of  the  oculo-motor  and  other  nerves  at  the  base  of  the  skull 
renders  the  nature  of  the  complication  more  apparent. 

Meningitis  ivith  Ulcerative  Endocarditis. — The  cerebral  symptoms 
in  ulcerative  endocarditis  are  caused  by  multiple  hemorrhagic  infarctions 
of  the  cortex  of  the  brain  or  of  the  pia  mater,  and  the  symptoms  pro- 
duced are  more  or  less  like  pyeemic  encephalitis. 

Rheumatic  meningitis  has  been  described,  but  post-mortem  evidence 
of  its  existence  is  wanting. 


(V.)  Traumatic  MENixiiiTis. 

Etiology. — This  form  of  meningitis  or  of  meningo-encephalitis  may 
appear  during  the  period  of  reaction  from  concussion,  or  follow  a  con- 
tusion of  the  brain.  Injury  of  the  scalp,  with  subsequent  inflammation 
of  the  bones  of  the  skull  and  dura  mater,  may  also  give  rise  to  inflam- 
mation of  the  pia  mater  and  brain.  At  other  times  the  inflammatory 
process  is  set  up  by  a  perforating  injury  of  the  skull  either  with  or 
without  extravasation  of  blood  between  the  dura  mater  and  the  bone, 
the  effects  in  such  cases  being  intensified  by  the  admission  of  air  con- 
taining germs  into  the  open  wound.  In  other  cases  the  meningitis  is  a 
secondary  result  of  osteitis,  thrombosis  of  the  sinuses  probably  playing 
an  important  part  in  its  production  in  such  cases.  The  meningitis  at 
other  times  may  result  after  necrosis  of  the  bone  has  taken  place. 
Hutchinson  thinks  that  in  fractures  of  the  petrous  portion  of  the 
temporal  bone  the  inflammation  extends  along  the  sheath  of  the  seventh 
nerve,  and  in  this  way  gains  access  to  the  subarachnoidal  spaces. 

Symptoms. — This  affection  may  be  divided  into  two  varieties :  (a) 
acute,  and  {h)  chronic  or  subacute  traumatic  meningo-encephalitis. 

{a)  Acute  Traumatic  Meningo-encephalitis.— The  symptoms  of  the 
onset  of  the  acute  form  of  the  affection  are  modified  by  the  fact  that 


()()()      DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

the  inflammatory  process  usually  attacks  a  patient  already  suffering 
from  the  symptoms  of  concussion,  compression,  or  contusion  of  the 
brain.  It  is  impossible  to  distinguish  between  the  symptoms  of  the 
reaction  period  of  concussion  and  those  of  the  early  or  congestive  stage 
of  true  inflammation,  so  that  we  are  unable  to  determine  when  the 
symptoms  of  the  former  terminate  and  those  of  the  latter  begin.  At 
the  onset  of  the  inflammatory  attack  the  patient  complains  of  severe 
and  continuous  cephalalgia ;  the  carotids  beat  forcibly ;  the  face  is 
suffused  and  the  scalp  hot ;  the  pupils  are  contracted ;  and  there  are 
intolerance  of  light  and  sound,  spectral  illusions,  noises  in  the  ears,  and 
general  hyperesthesia  to  external  impressions.  The  patient  likewise 
suff"ers  from  the  usual  symptoms  of  pyrexia  ;  the  pulse  is  full  and 
boundinij.  and  there  are  restlessness  and  wakefulness  with  delirium  of  a 
violent  character.  These  symptoms  may,  under  proper  treatment, 
gradually  subside  until  health  is  reestablished ;  but  more  commonly  the 
symptoms  of  the  stage  of  irritation  develop  into  those  of  the  stage  of 
compression. 

During  the  transition  period  between  the  early  stage  of  excitement 
and  that  of  comj)ression  of  the  brain,  the  symptoms  of  a  localized 
disease  may  make  their  appearance.  Clonic  or  tonic  spasms,  followed 
by  paralysis,  may  occur  in  particular  groups  of  muscles.  Rigidity  of 
the  muscles  of  the  nape  of  the  neck,  Avith  retraction  of  the  head,  is 
usually  present  at  this  period,  and  may  also  extend  to  the  muscles  of 
the  back  and  give  rise  to  tetanic  seizures.  Hemiplegia  of  the  side 
opposite  to  tlie  injury  is,  according  to  Hutchinson,  a  constant  symptom 
of  direct  traumatic  meningo-encephalitis.  Tlie  abdominal  muscles  are 
usually  retracted  and  the  bowels  constipated.  When  the  meningitis  is 
situated  at  the  base  of  the  brain,  the  cranial  nerves  in  their  passage 
along  the  base  of  the  skull  may  become  imj)licated.  The  most  usual 
symptoms  produced  are  ptosis,  strabismus,  paralysis  of  the  facial  muscles 
or  of  half  of  the  tongue,  and  difficulty  of  deglutition. 

The  symptoms  of  compression  of  the  brain  now  become  rapidly 
developed;  the  delirium  is  replaced  by  stupor,  from  which  the  patient 
is  roused  Avith  difficulty ;  the  pupils  are  dilated  and  insensible  to  light ; 
the  breathing  is  slow  and  stertorous  ;  the  pulse,  retarded  at  first,  becomes 
feeble  and  frequent  towards  the  end ;  the  skin  is  hot  and  bathed  in 
perspiration  ;  and  convulsive  twitchings  or  jerkings  of  the  limbs  are 
observed  ;  but  these  soon  give  place  to  general  muscular  relaxation,  and 
the  patient  dies  in  profound  coma. 

{b)  Subacute  Traumatic  Menhujo-encephalitiH. — This  form  of  men- 
ingo-encephalitis may  come  on  a  few  days  after  the  injury  or  not  until 
months  have  elapsed.     The  patient  has  often  apparently  recovered  from 


DISEASES    OF    THE    PIA    MATER.  667 

the  original  injury,  but,  as  a  rule,  some  of  the  consequences  of  con- 
cussion remain.  The  patient  in  the  interval  has  complained  of  head- 
ache, impairment  of  sight  and  hearing,  confusion  of  ideas,  or  mental 
in-itability.  The  symptoms  of  the  inflammatory  attack  may  be  ushered 
in  by  an  aggravation  of  the  symptoms  which  have  persisted  during  the 
interval,  or  by  an  epileptic  attack.  The  pupils  are  contracted,  dilated, 
or  unequal ;  there  are  intolerance  of  light  and  sound,  convulsive  twitch- 
ings  of  the  limbs  and  face,  strabismus,  delirium,  and  the  ordinary 
phenomena  of  symptomatic  fever.  After  a  time  the  symptoms  of  com- 
pression supervene,  and  the  patient  dies  comatose. 

Morbid  Anatomy. — In  external  pachymeningitis  the  dura  mater  is 
at  first  congested  and  presents  punctiform  extravasations,  while  at  a 
more  advanced  stage  the  membrane  becomes  swollen  and  infiltrated  with 
numerous  white  blood-corpuscles.  If  the  disease  has  been  acute,  the 
white  corpuscles  become  more  numerous  and  make  their  way  inwards, 
so  that  a  purulent  internal  pachymeningitis  is  superadded  to  the  external 
pachymeningitis.  If,  however,  the  disease  has  been  chronic,  the  Avhite 
blood-corpuscles  become  transformed  into  spindle-cells  and  ultimately 
develop  into  connective  tissue.  In  long-standing  cases  portions  of  the 
membrane  may  become  calcified. 

HemorrJiagie  pachymeningitis  appears  to  begin  with  hypergemia  of 
the  dura  mater  in  the  'area  of  distril)ution  of  the  middle  meningeal 
artery.  The  inner  surface  of  the  dura  mater  assumes  a  rosy  color,  and 
after  a  time  a  loose  yellowish  coating  or  false  membrane  forms,  which 
is  dotted  with  a  number  of  confluent  or  separate  hemorrhagic  points. 
The  false  membrane  become  very  vascular  and  from  time  to  time  some 
of  them  rupture,  giving  rise  to  hemorrhages  of  variable  quantity.  The 
clots  which  form  become  partially  organized  and  the  delicate  capillaries 
which  develop  in  them  become  the  source  of  new  hemorrhages,  so  that 
in  this  way  a  large  quantity  of  blood  may  be  poured  out  between  the 
thickened  membranes.  Haematoma  is  most  frequently  found  in  the 
upper  part  of  the  brain  along  the  falx  cerebri  and  thence  it  spreads 
down  the  curved  portion  of  the  frontal  and  occipital  lobes  and  later- 
ally towards  the  Sylvian  fissure.  The  bones  of  the  skull  have  been 
found  sometimes  abnormally  thin  and  at  other  times  unusually  thick, 
and  the  brain  itself  is  compressed  by  the  hnematoma,  while  it  is  often 
the  subject  of  atrophy  independently  of  the  disease  in  tlie  membranes. 

In  tubercular  meningitis  the  changes  in  the  pia  mater  are  (1)  those 
which  are  directly  connected  with  the  formation  of  tubercles,  (2)  those 
caused  by  the  inflammation  surrounding  them,  and  (3)  those  which  arise 
from  the  effusion  into  the  ventricles. 


668       DISEASES    OF    THE    MEMBRANES    OF    THE    BRAIN. 

(1)  The  pia  mater  is  studded  with  tubercles  which  appear  as  grayish- 
white  granulations  distributed  along  the  course  of  the  vessels,  the  terri- 
tory supplied  by  the  Sylvian  artery  being  particularly  liable  to  be 
affected. 

(2)  The  inflammatory  changes  in  the  pia  mater  vary  greatly  accord- 
ing to  the  amount  of  effusion  which  has  been  present.  Evidences  of 
suppuration  are  found  at  the  base  of  the  brain,  and  cloudy  streaks  of 
exudation  may  be  observed  passing  along  the  vessels.  In  some  cases  a 
purulent  or  fibrinous  effusion  is  observed  in  the  pia  mater  of  the  con- 
vexity, which  may  extend  backwards  over  the  anterior  surface  of  the 
pons  and  medulla  and  find  its  Avay  over  the  entire  surface  of  the  cere- 
bellum. In  some  cases  the  choroid  plexuses  and  the  velum  interpositum 
are  covered  with  a  yellowish  purulent  exudation. 

(3)  The  ventricles  are  generally  distended  with  serous  or  sero-puru- 
lent  fluid,  and  the  brain  is  compressed,  so  that  the  cortex  and  white  sub- 
stance are  dry  and  ansemic,  but  when  effusion  is  absent  those  parts  are 
congested  and  oedematous. 

The  cortex  is  often  studded  by  punctiform  hemorrhages  caused,  accord- 
ing to  Rindfleiscli,  by  tubercular  degeneration  of  the  nutritive  arteries. 
AVhen  the  exudation  sj)reads  along  the  base  of  the  brain  the  cranial 
nerves  are  implicated  in  the  disease,  and  even  the  spinal  cord  is  not 
unfrequently  affected. 

Essentially  the  same  phenomena  are  met  with  in  the  other  forms  of 
acute  meningitis  as  in  the  tubercular  variety,  so  far  as  the  appearances 
of  inflammation  and  the  effusion  are  concerned,  and  it  is,  therefore, 
unnecessary  to  describe  the  morbid  changes  of  these  diseases  in  detail. 

In  chronic  hydrocephalus  the  general  ventricular  cavity  of  the  brain 
contains  serous  fluid,  which  varies  in  quantity  from  a  few  ounces  to  many 
pounds,  and  conse([uently  the  hemis])heres  of  tlie  brain  are  compressed 
and  flattened,  so  that  the  sulci  and  convolutions  almost  entirely  disappear. 

Morbid  Physiology. — The  premonitory  symptoms  of  all  the  acute 
forms  of  meningitis  are  such  as  are  met  with  in  all  severe  inflammatory 
affections,  and  the  purely  nervous  phenomena  of  the  period  of  invasion 
are  caused  by  irritation  of  the  cortex  of  the  brain,  and  the  student  who 
is  acquainted  with  the  physiology  of  the  cortex  will  be  able  readily  to 
explain  the  various  sensory  disorders  and  the  spasmodic  affections  which 
occur  at  this  period  of  the  disease.  In  the  second  stage  of  the  disease 
portions  of  the  structure  of  the  cortex  are  being  destroyed,  so  that  the 
hyperaesthesias  and  spasms  of  the  first  period  become  mixed  up  with 
various  forms  of  anaesthesia  and  paralysis.  Direct  implication  of  the 
cranial  nerves  in  the  inflammatory  process  at  the  base  of  the  brain 
explains  some  of  the  local  forms  of  anaesthesia  and  paralysis  which 


DISEASES    OF    THE    PIA     MATER.  669 

occ'iu-  at  this  period.  As  the  eftusion  increases  in  quantity  the  brain  is 
subjected  to  compression  and  its  functions  are  gradually  or  suddenly 
abolished,  and  the  patient  dies  comatose. 

Treatment. — The  treatment  of  all  the  acute  forms  of  meningitis  must 
be  conducted  on  the  same  general  principles,  by  the  application  of  ice 
to  the  shaven  scalp,  rest  in  a  darkened  room,  and  moderate  evacuation 
of  the  bowels  by  a  saline  purgative.  Local  bloodletting  often  relieves 
the  severe  headache  and  gives  at  least  temporary  relief. 

In  external  pachymeninyith  the  question  of  trephining  will  arise 
Avhen  an  abscess  forms  or  an  extravasation  of  blood  takes  place  between 
the  dura  mater  and  bone,  but  such  cases  come  under  the  care  of  the 
surgeon. 

In  licematoma  the  treatment  will  depend  greatly  upon  the  underlying 
affection,  and  a  careful  examination  must  be  made  into  the  habits  of  the 
patient,  and  of  all  the  other  organs,  in  order  to  discover  upon  what 
disease  the  meningeal  affection  depends. 

In  all  the  acute  inflammations  of  the  pia  mater  mercury  may  be  given 
in  frequently  repeated  small  doses ;  in  the  tubercular  disease  this  treat- 
ment can  do  no  harm,  and  in  the  simple  varieties  it  may  do  good.  Iodide 
of  potassium  has  also  been  given  with  the  view  of  promoting  absorption 
of  the  effusion  but  the  results  of  this  treatment  are  doubtful.  When 
the  headache  is  very  severe,  morphia  in  suitable  doses  should  be  admin- 
istered subcutaneously,  and  chloral  hydrate  and  l)romide  of  potassium 
either  separately  or  combined  will  be  found  useful  when  the  convulsive 
symptoms  are  severe.  Blisters  or  croton  oil  liniment  to  the  shaven 
scalp  have  been  much  used  in  the  treatment  of  meningitis,  but  I  cannot 
too  strongly  condemn  this  practice. 

In  chronic  hydrocephalus  partial  success  has  been  obtained  by  with- 
draw^ing  a  few  ounces  of  fluid  at  a  time  by  means  of  an  aspirator,  while 
the  skull  is  at  the  same  time  supported  by  bandages. 


CHAPTEE    XX.  j 

PARALYSIS  AGITANS,  MULTIPLE  SCLEROSIS.  AND  CHOREA. 

I.  PAEALYSIS  AGITANS. 

Etiology. — Paralysis  agitans  occurs  generally  in  advanced  age, 
although  a  few  cases  have  been  observed  in  young  people.  Men  are 
more  frequently  attacked  than  women.  The  disease  is  frequently  met 
with  amongst  persons  living  in  damp  and  unhealthy  situations,  and 
some  authors  believe  that  there  is  a  causal  relation  between  it  and 
rheumatism.  It  is  sometimes  caused  by  great  emotional  disturbance, 
and  many  cases  follow  wounds  and  other  injuries. 

Symptoms. — The  clinical  history  of  paralysis  agitans  may  be  divided 
into  three  stages:  (1)  The  period  of  invasion;  (2)  the  stationary 
period;  and  (3)  the  terminal  period. 

(1)  The  Period  of  Invasion. — Paralysis  agitans  may  begin  in  a 
slow  and  progressive  manner,  or  more  or  less  suddenly.  In  the  sloiu 
mode  of  invasion  the  characteristic  jihenomena  of  the  disease  are  pre- 
ceded by  premonitory  symptoms,  consisting  of  sleeplessness,  mental 
irritability,  rheumatoid  or  neuralgic  pains,  a  remarkable  feeling  of 
fotigue,  and  a  transitory  feeling  of  Aveakness  in  the  limbs.  After  a  longer 
or  shorter  time  the  disease  declares  itself  by  a  trembling  in  one  of  the  ex- 
tremities, generally  in  the  small  muscles  of  one  hand.  At  first  the  tremor 
is  only  occasionally  })resent,  but  as  the  disease  advances  it  becomes  per- 
sistent during  w'aking  hours,  but  ceases  with  sleep,  and  it  can  be  arrested 
by  a  strong  voluntary  effort.  When  the  hand  is  the  first  part  affected, 
the  "patient,"  to  quote  Charcot,  "closes  the  fingers  on  the  thumb,  as 
though  in  the  act  of  spinning  wool,  at  the  same  moment  the  wrist  is 
bent  by  rapid  jerks  on  the  forearm  and  the  forearm  on  the  arm.'  As 
the  disease  advances,  the  tremor  increases  in  intensity  and  persistency, 
and  invades  by  degrees  parts  which  have  hitherto  remained  sound. 
The  order  in  which  the  tremor  invades  the  different  groups  of  muscles 
is  somewhat  variable.  In  some  cases  the  tremor  is  restricted  for  a  long 
time  to  one-half  of  the  body,  the  tremor  begins  in  the  right  hand,  and 
after  months  or  years  the  lower  extremity  on  the  same  side  becomes 
affected,  and  after  another  variable  i)eriod  the  left  hand  and  foot  are 


SYMPTOMS.  671 

successively  invaded.  In  other  cases  both  lower  extremities  are  first 
aftected,  and  in  a  few  cases  the  upper  extremity  of  the  one  side,  (gener- 
ally the  right,  is  first  attacked,  and  then  the  lower  extremity  of  the 
opposite  side. 

In  the  sudden  mode  of  invasion  the  tremor  appears  suddenly  either 
in  one  extremity  or  in  all  the  limbs  at  once;  it  may  soon  diminish  or 
disappear,  but  soon  recurs,  and  after  a  series  of  alternate  exacerbations 
and  remissions,  becomes  permanent.  The  duration  of  the  initial  stage 
varies  from  one  to  three  years. 

(2)  Stationary  Period. — When  the  disease  is  fully  developed  the 
trembling  becomes  almost  incessant,  although  it  varies  in  intensity. 
It  is  aggravated  by  emotional  excitement,  cold,  and  voluntary  efi'ort, 
and  becomes  less  during  repose,  and  ceases  during  sleep.  The  diiferent 
segments  of  the  fingers  and  hand  undergo  involuntary  and  rh^^thmical 
oscillations,  which  closely  resemble  voluntary  movements.  "Thus  in 
some  patients,"  says  Charcot,  "the  thumb  moves  over  the  fingers  as 
when  a  pencil  or  paper  ball  is  rolled  between  them;  in  others  the 
movements  are  more  complicated,  and  resemble  what  takes  place  in 
crumbling  a  piece  of  bread."  The  handwriting  now  assumes  special 
characteristics.  At  an  early  stage  of  the  disease  the  writing  at  the  first 
glance  presents  little  change,  but  when  examined  with  a  magnifying 
glass  slight  inequalities  are  perceived,  and  as  the  disease  advances  the 
up-strokes  become  markedly  tremulous. 

The  muscles  of  the  head  and  neck,  as  already  stated,  usually  remain 
unaffected.  The  muscles  of  the  eyeballs  are  also  exempt  from  tremor, 
and  consequently  nystagmus,  Avhich  is  so  prominent  a  symptom  of  dis- 
seminated sclerosis,  has  no  existence  in  paralysis  agitans.  Tlie  move- 
ments of  the  eyeballs  are,  however,  often  executed  with  great  slowness. 
The  muscles  of  the  face,  instead  of  trembling,  are  motionless ;  the  features 
become  fixed;  and  the  face  assumes  a  mournful,  stolid,  or  vacant  ex- 
pression. The  utterance  is  slow,  jerky,  and  accomplished  with  great 
apparent  effort,  soon  inducing  weariness,  and  if  the  tremor  of  the  body 
be  intense  it  becomes  tremulous  and  broken,  while  in  old-standing 
cases  the  saliva  may  dribble  from  the  mouth  to  some  extent. 

After  a  longer  or  shorter  time  the  muscular  power  becomes  gradually 
weakened.  In  many  cases,  however,  motor  weakness  is  more  apparent 
than  real,  the  phenomena  depending  upon  the  great  slowness  with 
which  voluntary  movements  are  executed,  the  immense  effort  which  all 
voluntary  actions,  even  speaking,  entail,  and  the  readiness  with  which 
fatigue  is  induced.  But  although  the  muscular  power,  when  measured 
by  the  dynamometer,  is  often  retained  much  longer  than  might  be 
expected,  yet  after  a  time  motor  power  becomes  gradually  diminished,  and 


672  PARALYSIS    AGITANS. 

paralytic  symptoms  supervene.  The  paralysis,  however,  almost  always 
remains  partial,  and  is  irregularly  developed  in  different  groups  of 
muscles,  and,  as  in  various  other  forms  of  paralysis,  the  extensors  of 
the  limbs  are  affected  to  a  greater  extent  than  the  flexors.  The  trem- 
blino-  often  abates  in  the  muscles  as  paralysis  increases.  The  bladder 
and  rectum  are  only  very  exceptionally  involved  in  the  paralysis.  The 
muscles  react  normally  to  both  the  faradic  and  galvanic  currents. 

After  a  time  the  muscles  of  the  extremities,  trunk,  and  neck  become 
the  subjects  of  rigidity,  at  first  temporary,  but  ultimately  becoming 
permanent,  the  flexors  being  affected  to  a  greater  extent  than  the  ex- 
tensors. The  rigidity  of  the  muscles  produces  characteristic  alterations 
in  the  attitudes  of  the  body.  The  rigidity  of  the  anterior  cervical 
muscles  causes  the  head  to  be  strongly  bent  forwards,  and  the  patient 
cannot  raise  it  or  turn  it  to  either  side  without  great  difiiculty.  The 
body  is  also  inclined  forwards  Avhen  the  patient  is  standing.  The 
elbows  are  habitually  held  somewhat  removed  from  the  chest,  the  fore- 
arms are  slightly  flexed  on  the  arms,  and  the  hands  are  sometimes 
flexed,  sometimes  slightly  extended  on  the  forearms,  and  rest  on  the 
epigastrium.  The  fingers  are  flexed  at  the  metacarpo-phalangeal  articu- 
lations, the  index  and  middle  fingers  are  extended,  but  the  remaining 
fingers  are  slightly  flexed  at  the  phalangeal  articulations,  all  of  them 
are  slightly  inclined  to  the  ulnar  border  of  the  hand,  and  the  thumb  is 
extended  and  opposed  to  the  index  finger,  so  that  the  attitude  of  the 
hand  and  fingers  closely  resembles  that  assumed  by  tliem  in  holding  a 
pen  (Fig.  179).     In  some  cases  the  fingers  are  alternately  flexed  and 

Fig   170. 


Attitude  ok  the  IIand  in  I'arai.ysis  Aoitans.     (After  ('iiaucot.) 

extended  at  their  several  articulations  so  as  to  resemble  the  distortions 
of  arthritis  deforinans  (Fig.  1(S0).  In  paralysis  agitans,  however,  the 
joints  are  not  swollen  and  stift",  and  passive  movement  of  the  articula- 
tions does  not  give  rise  to  the  creaking  sounds  observed  in  the  rheumatic 
affection.  The  rigidity  of  the  muscles  of  the  lower  extremities  is  some- 
times so  great  as  to  resemble  paraplegia  with  contracture.     The  spasm 


SYMPTOMS.  673 

of  the  adductors  of  the  thighs  and  muscles  of  the  calf  predominates 
over  their  antagonists,  so  that  the  knees  are  drawn  inwards,  the  leo-  is 
slightly  flexed  on  the  thigh,  and  the  foot  assumes  the  well-known  posi- 
tion of  talipes  equino-varus.  The  toes  are  extended  at  the  metatarso- 
phalangeal and  flexed  at  the  phalangeal  articulations  [Griff e  des  Orteih). 

Fro.  180. 


Attiti'de  or  THE  }1am)  IX  Paralysis  Agitans  simvlating  that  of  Authritis  Deformans. 

(Alter  Charcot.) 

In  the  advanced  stage  of  this  disease  the  patients  move  all  of  a  piece, 
as  if  their  joints  were  soldered  together,  and  the  head  and  body  are 
kept  inclined  forwards,  a  position  which  no  doubt  largely  contributes 
to  produce  that  tendency  to  fall  forwards  manifested  when  walking. 

The  gait  is  now  characteristic.  The  patient  gets  up  sloAvly  and  with 
difficulty  from  his  seat,  and  hesitates  for  a  few  moments  before  starting; 
Avhen  once  he  has  begun  to  walk,  he  is  compelled  to  run  forwards,  in 
order  to  save  himself  from  falling.  In  the  language  of  Trousseau,  he 
looks  as  if  pursuing  his  own  centre  of  gravity.  This  gait  has  been 
called  parali/sis  festinans  or  procursoria,  or  slmiplj  propulsion. 

The  forward  running  or  propulsion  is  the  usual  gait  of  paralysis 
agitans,  but  some  patients  manifest  a  strong  tendency  to  run  or  to  fall 
backwards,  although  their  bodies  are  inclined  forwards,  a  tendency 
which  has  been  named  retropulsion.  Graves  mentions  the  case  of  a 
patient  who,  if  arrested  in  his  forward  movement,  immediately  began  to 
run  backwards,  and  Chai'cot  could  excite  the  impulse  to  move  back- 
wards in  a  female  patient  by  slightly  pulling  her  back  by  the  dress 
when  slie  was  standing.  It  has  already  been  mentioned  that  a  few 
cases  of  paralysis  agitans  are  ushered  in  by  rheumatoid  or  neuralgic 
pains,  but  in  the  majority  of  cases  pains  are  absent.  The  patient  is, 
however,  distressed  by  disagreeable  sensations,"  such  as  cramps  and  sensa- 
tions of  tension  and  traction  in  the  muscles,  along  with  a  general  feeling 
of  weariness  and  discomfort.  These  sensations  render  the  patient  restless, 
and  cause  him  to  seek  frequent  changes  of  posture.  He  complains  of 
a  constant  sensation  of  excessive  heat,  although  the  thermometer  shows 
that  the  temperature  of  the  body  is  normal.     In  order  to  relieve  this 

43 


674  MULTIPLE    SCLEROSIS. 

feeling  the  patient  throws  off  the  bedclothes  at  night,  and  only  retains 
the  lightest  garments  in  the  daytime.  This  sensation  of  heat  is  espe- 
cially felt  in  tlie  epigastrium  and  back,  but  may  affect  the  face  and 
limbs.  It  is  liable  to  remissions  and  exacerbations,  and  seems  to  attain 
its  maximum  after  a  paroxysm  of  trembling ;  it  is  often  accompanied  by 
profuse  perspiration. 

(3)  Terminal  Period. — The  course  of  the  disease  is  very  protracted, 
and  may  extend  over  a  period  of  many  years.  As  the  tremors  and 
muscular  rigidity  increase  in  intensity,  the  patients  are  compelled  to 
remain  the  whole  day  seated  on  a  chair,  or  confined  to  bed.  The  general 
nutrition  suffers,  the  muscles  become  atrophied,  and  the  paresis  of  the 
second  stage  of  the  disease  gives  place  to  pronounced  paralysis.  The 
memory  and  intellect  are  weakened,  general  prostration  sets  in,  the 
urine  and  feces  are  passed  unconsciously,  bedsores  appear  on  the  sacrum, 
and  the  patient  dies  from  nervous  exhaustion  and  marasmus.  The 
tremors  disappear  entirely  a  few  days  before  death,  and  paralytic  symp- 
toms become  predominant.  In  the  majority  of  cases,  however,  death 
results  from  some  intercurrent  disease,  sucli  as  pneumonia  or  pleurisy. 


II.   MULTIPLE    SCLEROSIS   OF   THE    BKAIN    AND    Sl'INAL    CORD 
(DISSEMINATED   OR   INSULAR   SCLEROSIS). 

Etiology. — Hereditary  transmission  has  been  traced  in  several  re- 
corded cases  of  multiple  sclerosis,  although  it  is  always  indirect  rather 
than  direct.  It  is  commonly  observed  in  youth  and  middle  age,  and  a 
considerable  proportion  of  the  cases  recorded  in  p]ngland  have  been  in 
children  under  ten  years  of  age.  It  is  probably  more  frequent  in 
women  than  in  men,  but  the  disproportion  between  the  sexes  is  probably 
not  great.  The  exciting  causes  are  exposure  to  cold  and  damp,  excessive 
mental  or  bodily  exertion,  profound  emotional  disturbances  and  trau- 
matic influences,  as  blows  on  the  head  and  concussion  from  railway 
accidents. 

Symptoms. — Multiple  sclerosis  may  be  divided  into  three  varieties: 
(1)  the  cerebrospinal,  (2)  the  cerebral,  and  (3)  the  spinal  form.  Of 
these  the  cerebro-spinal  variety  is  by  far  the  most  fre(iuent  and  important. 

(1)  The  Cerebro-spinal  Form. — This  form  of  multiple  sclerosis  may 
develop  gradually  and  insidiously  or  suddenly.  In  cases,  the  develop- 
ment of  Avhich  is  gradual,  the  initial  symptoms  are  very  obscure,  and 
may  be  referred  either  to  the  spinal  cord  or  brain.  The  spinal  symp- 
toms which  usher  in  the  disease  consist  of  paresis  of  the  lower  extremities, 
with  a  slow  and  trembling  gait,  or  ataxia  with  various  parsesthesioe, 
neuralgic   pains,  other  disturbances  of  sensibility  in  the  limbs,  and 


SYMPTOMS.  675 

cardialgic  attacks  accompanied  by  urgent  vomiting.  The  more  usual 
cerebral  symptoms  observed  in  the  beginning  of  the  disease  are  vertigo, 
headache,  staggering  gait,  tremors  on  voluntary  effort,  impairment  of 
speech,  vision,  or  hearing,  paresis  of  the  muscles  supplied  by  one  or 
more  of  the  cranial  motor  nerves,  and  various  psychical  disturbances. 
When  the  disease  begins  abruptly,  the  symptoms  are  ushered  in  by  a 
convulsive  or  apoplectiform  attack,  followed  by  diplopia,  amblyopia, 
nystagmus,  and  disturbances  of  speech. 

The  first  motor  symptom  to  attract  attention  is  usually  paresis  or 
paralysis  of  certain  muscular  groups.  Weakness  generally  begins  in 
one  leg,  and  subsequently  extends  to  the  other  leg  and  to  the  arms,  but 
the  order  in  which  the  paralysis  of  the  difterent  muscular  groups  is 
developed  presents  every  imaginable  combination. 

The  gait  is  usually  of  the  spastic  variety,  muscular  contractures  set 
in,  and  the  legs  are  held  like  rigid  bars  in  the  position  of  extension  and 
adduction,  just  as  in  primary  lateral  sclerosis.  In  the  later  stages  of 
the  disease  flexion  of  the  different  segments  of  the  lower  extremities 
may  predominate  over  extension.  The  paralysis  rarely  becomes  so  well 
marked  in  the  upper  as  in  the  lower  extremities.  When  the  upper 
extremities  are,  however,  affected  with  paralysis  and  contracture,  they 
are  maintained  in  a  position  of  forced  extension,  and  closely  applied  to 
the  sides  of  the  body.  The  affection  sometimes  begins  with  ataxia,  but 
in  these  cases  it  may  often  be  noticed  that  characteristic  symptoms  of 
true  locomotor  ataxia  are  absent,  while  others  are  present  which  do  not 
usually  belong  to  it. 

Intermittent  muscular  tremor  constitutes  one  of  the  most  character- 
istic symptoms  of  this  affection,  although  it  has  been  found  absent  in  a 
few  isolated  cases.  This  tremor  appears  almost  exclusively  during 
voluntary  movements,  and  disappears  during  repose.  So  long  as  the 
patient  remains  seated  quietly  the  tremor  is  either  entirely  absent,  or 
at  most  there  is  only  a  trifling  shaking  movement  of  the  head,  or  a  slight 
oscillation  of  the  trunk.  As  soon,  however,  as  he  attempts  to  seize 
anything  with  his  hand  the  tremor  begins,  and  increases  in  violence  in 
proportion  to  the  effort  made  to  execute  the  movement.  Several  devices 
may  be  used  in  order  to  bring  into  prominence  the  characteristic  tremor 
(if  multiple  sclerosis,  such  as  asking  the  patient  to  seize  small  objects 
with  his  fingers  or  to  stretch  out  his  arms  horizontally  before  him. 

The  tremor  of  this  affection  differs  from  that  of  paralysis  agitans, 
not  only  in  being  intermittent  instead  of  continuous,  but  also  in  having 
a  much  wider  sweep  than  that  of  the  latter  affection.  It  holds  an 
intermediate  position  between  the  extensive  jerking  movements  of 
chorea,    and  the  small  and  frequent  oscillations  of  paralysis  agitans. 


676  MULTIPLE    SCLEROSIS. 

The  true  characteristic  of  the  tremor  of  multiple  sclerosis  is  best  elicited 
by  asking  the  patient  to  convey  a  glass  of  water  to  his  mouth.  As  the 
glass  is  being  carried  to  the  mouth  it  oscillates  from  side  to  side  in  the 
patient's  hand,  these  oscillations  appearing  to  increase  in  extent  and 
frequency  as  the  mouth  is  approached.  In  aggravated  cases  the  con- 
tents of  the  glass  are  spilt  in  every  direction ;  but  in  milder  cases  the 
patient  is  able,  by  moving  his  head  downwards  in  ordei"  to  meet  the 
glass,  to  apply  it  to  his  lips,  and  then  the  trunk,  head,  and  arms  begin 
to  tremble  violently,  so  that  the  edge  of  the  glass  rattles  against  the 
teeth,  and  the  contents  are  spluttered  over  the  patient's  face.  When 
the  patient  rises  and  attemj)ts  to  walk  the  tremor  involves  the  entire 
body,  which  may  be  shaken  with  such  violence  that  he  is  unable  to  pro- 
ceed or  even  to  remain  standing.  As  soon  as  the  voluntary  effort  is 
relaxed  the  tremor  diminishes,  and  as  long  as  the  patient  is  in  tlie 
recumbent  posture  no  trace  of  it  can  usually  be  detected ;  occasionally 
the  tremor  has  been  known  to  persist  during  repose. 

The  sensory  disturl)ances  are  somewhat  variable  and  not  always  well 
marked.  They  may  assume  the  form  of  facial  neuralgia,  lancinating 
or  diffused  pains  in  the  extremities,  hyperesthesia  or  anaesthesia  of 
variable  distribution,  girdle  jtains.  and  various  j)arpestliesiic  felt  in  dif- 
ferent parts  of  the  body,  the  latter  being  the  most  frequent  of  all  the 
sensory  disorders. 

The  reflex  actions  are  variously  affected  in  different  cases.  The 
cutaneous  reflexes  remain  for  a  long  time  unaffected:  but  the  tendon- 
reactions  are  usually  exaggerated,  especially  in  the  lower  extremities. 
In  consequence  of  the  increase  of  the  tendon-reactions  in  the  lower  ex- 
tremities, the  knee-phenomenon  and  ankle-clonus  are  usually  exaggerated, 
and  the  limbs  may  be  thrown  into  the  state  of  trembling  named  spinal 
epilepsy.  This  condition  must,  however,  be  carefully  distinguished  from 
the  characteristic  tremor  of  multiple  sclerosis. 

Trophic  disturbances  are  generally  wanting  for  a  long  time,  but  in  the 
later  stages  various  nutritive  disorders  usually  make  their  appearance. 
The  sclerotic  nodules  may  encroach  on  the  anterior  gray  horns  of  the 
spinal  cord,  and  then  muscular  atrophy  results  as  in  progressive  muscular 
atrophy.  Muscular  atrophy  may  present  itself  in  the  upper  or  lower 
extremities,  neck,  face,  tongue,  or  indeed  in  any  part  of  the  body.  The 
electrical  reactions  of  the  nerves  and  muscles  remain  normal  until  the 
muscular  atrophy  begins,  and  then  the  electric  irritability  of  both 
becomes  gradually  diminished. 

During  the  terminal  period  of  the  disease  bedsores  appear  over  the 
sacrum  and  other  parts  subjected  to  pressure,  and  general  nutrition  fails. 

The  bladder  and  rectum,  as  a  rule,  remain  unaffected  for  a  compara- 


SYMPTOMS.  677 

tively  long  time,  but  their  functions  are  ultimately  interfered  with  as  in 
chronic  myelitis.  The  disorders  of  the  sexual  functions  are  somewhat 
variable.  In  some  patients  sexual  desire  appears  to  be  increased  at  an 
early  period  of  the  disease,  while  in  others  it  is  completely  abolished. 
In  the  majority  of  cases  the  sexual  functions  remain  normal  for  a  com- 
paratively long  time. 

Bulbar  Symptoms. — Some  of  the  phenomena  caused  by  implication 
of  the  pons  and  medulla  oblongata  in  the  morbid  process  are  amongst 
the  most  important  and  characteristic  symptoms  of  the  disease.  The 
speech  is  slow  and  hesitating,  while  each  syllable  is  separately  pro- 
nounced, presenting  a  mode  of  articulation  which  has  been  named  the 
syllabic  or  scanning.  The  voice  is  weak,  low,  sometimes  whispering, 
and  monotonous,  while  it  breaks  readily  when  forced  efforts  are  made. 
Laryngoscopic  examination  shows  that  the  vocal  cords  move  normally, 
but  their  tension  is  diminished  and  frequently  changes.  The  acts  of 
laughing  and  crying  are  often  represented  by  peculiar  noisy  inspirations. 
After  a  time  symptoms  of  true  bulbar  paralysis  supervene,  the  move- 
ments of  the  lips  and  tongue  are  impaired,  and  by-and-by  mastication 
and  deglutition  become  increasingly  difficult,  the  velum  palati  is  para- 
lyzed, speech  becomes  inarticulate,  and  the  mouth  remains  permanently 
paralyzed,  while  the  saliva  dribbles  out. 

Diplopia  with  strabismus  is  a  not  unfrequent  symptom,  although  it 
may  subsequently  disappear  as  in  locomotor  ataxia. 

Nystagmus  is,  however,  the  most  important  of  all  the  ocular  symp- 
toms, being  present,  according  to  Charcot,  in  about  half  the  cases. 
The  movements  of  the  eyeballs  may  be  persistent  or  occur  only  during 
forced  accommodation,  or  when  movements  are  performed  by  the  ex- 
tremities. At  other  times  the  nystagmus  may  not  be  apparent  during 
the  ordinary  movements  of  the  eyeballs,  but  when  the  patient  is  asked 
to  look  upwards  and  outwards  so  as  to  strain  the  ocular  muscles,  slight 
oscillatory  movements  may  be  observed. 

Amblyopia  or  amaurosis  is  a  frequent  symptom.  Of  fifty  cases 
observed  by  Guanck,  defects  of  vision  were  found  in  twenty-eight  cases, 
and  of  these  cases  various  degrees  of  amblyopia  were  present  in  eight, 
amblyopia  and  restriction  of  the  field  of  vision  with  dyschromatopsia  in 
five,  and  amblyopia  and  defects  of  the  field  of  vision,  with  morbid  changes 
in  the  optic  disks,  in  fifteen  cases.  Of  the  fifteen  cases  in  which  the  optic 
disks  were  found  altered,  complete  white  atrophy  of  both  disks  with  blind- 
ness was  found  in  two  cases.  Such  cases  are  rare,  the  rule  being  that 
atrophy  of  the  optic  nerve  in  multiple  sclerosis  is  unilateral.  In  ten 
cases  partial  white  atrophy  was  observed,  the  change  in  color  was  strictly 
limited  to  the  temporal  halves  of  the  fields  of  vision  in  four  cases,  while 


678  MULTIPLE    SCLEROSIS. 

the  nasal  halves  were  affected,  but  in  a  much  less  degree  than  the  tem- 
poral halves,  in  six  cases.  In  the  remaining  three  cases  hypersemia  of 
the  disks  with  optic  neuritis  was  present,  caused,  most  probably,  by  a 
retrobulbar  neuritis.  The  senses  of  smell,  taste,  and  hearing  are  im- 
paired in  some  cases,  but  these  disorders  are  rare. 

Psychical  disorders  are  always  observed  in  multiple  cerebro-spinal 
sclerosis.  They  consist  of  mental  irritability,  emotional  excitement 
causing  the  patient  to  laugh  or  to  shed  tears  without  apparent  motive, 
and  impairment  of  memory  and  intelligence.  At  other  times  the 
mental  disorder  assumes  the  form  of  distinct  unsoundness  of  mind. 
In  such  cases  there  may  be  melancholia,  monomania,  with  ideas  of  per- 
secution or  of  grandeur,  and  tlie  patient  may  fall  into  a  state  of  com- 
plete dementia. 

In  the  course  of  the  disease,  the  patient  suffers  from  attacks  of 
vertigo.  This  symptom  usually  comes  on  at  an  early  period,  and  con- 
tinues to  distress  the  patient  throughout.  The  patients  feel  as  if  they 
themselves  were  being  turned  round,  or  as  if  surrounding  objects  were 
whirling  around  them.  They  suffer  greatly  from  sleeplessness  and 
violent  headache. 

Apoplectiforin  or  epileptiform  seizures  have  been  observed  in  a  small 
number  of  cases ;  they  are  apparently  analogous  to  the  apoplectiform 
attacks  which  occur  in  general  paralysis  of  the  insane.  They  are 
characterized  by  the  development  of  grave  cerebral  symptoms,  and  are 
accompanied  by  a  considerable  elevation  of  temperature.  After  slight 
premonitory  symptoms,  such  as  a  feeling  of  pressure  in  the  head,  there 
is  a  partial  loss  of  consciousness,  which  in  a  few  hours  may  develoj) 
into  coma.  The  face  is  red  and  hot,  the  pulse  is  quick,  and  the  tem- 
perature of  the  body  rises  to  104°  F.  or  105°  F.  In  most  cases  hemi- 
plegia with  muscular  flaccidity,  and  on  rare  occasions  rigidity,  is 
present  from  the  outset  of  the  seizure.  After  one  or  two  days  the 
temperature  falls,  the  patient  sinks  into  a  quiet  sleep  from  which  he 
may  be  readily  roused,  and  he  feels,  on  awaking,  comparatively  well. 
Hemiplegia,  hov/ever,  persists  for  a  few  days  longer,  and  then  gradu- 
ally disappears.  These  attacks  may  be  repeated  several  times  in  the 
course  of  the  disease,  recurring  in  some  cases  every  few  months,  but 
each  is  followed  by  an  aggravation  of  the  general  symptoms,  and  death 
sometimes  occurs  during  an  attack. 

(2)  Cerebral  Multiple  Sclerosis. — In  this  form  of  the  disease,  which 
is  rarely  observed,  the  psychical  disturbances  are  predominant.  The 
tremor  is  said  to  precede  the  paralytic  manifestations,  but  in  other 
respects  the  course  of  the  affection  does  not  differ  greatly  from  the 
cerebro-spinal  variety. 


C  H  O  K  E  A .  679 

(8)  Spinal  Multiple  Sclerosis. — The  spinal  fonii  of  the  affection  is 
characterized  by  absence  of  the  cerebral  symptoms,  particularly  nys- 
tagmus, tremor  on  voluntary  effort,  vertigo,  apoplectiform  attacks,  and 
psychical  disturbances.  The  symptoms  of  the  spinal  form  of  multiple 
sclerosis  often  simulate  those  of  a  primary  lateral  sclerosis,  amyotrophic 
lateral  sclerosis,  or  locomotor  ataxia,  but  in  the  first  disease  symptoms 
are  usually  superadded  Avhich  do  not  belong  to  the  symptoms  of  the 
classical  forms  of  the  last  three  diseases.  The  course  of  multiple 
sclerosis  is  somewhat  variable,  the  average  duration  being  from  five  to 
ten  years.  The  first  stage  extends  from  the  commencement  of  the 
symptoms  up  to  the  appearance  of  marked  paralysis  with  contractures. 
This  stage  occasionally  begins  Avith  cerebral  symptoms,  consisting  of 
headache,  vertigo,  and  unsteady  gait,  but  most  commonly  it  commences 
■with  paresis  of  the  lower  extremities  like  that  caused  by  a  primary 
lateral  sclerosis,  and  in  such  cases  the  nature  of  the  disease  may  not  be 
recognized  until  the  appearance  of  the  characteristic  tremor.  In  other 
cases  the  disease  begins  by  an  apoplectiform  attack  or  gastralgic  dis- 
turbances, while  paralyses,  disorders  of  coordination,  tremor,  and  other 
symptoms  are  added  in  (juick  succession.  The  progress  of  this  stage  is 
often  interrupted  by  remissions  or  improvements,  but  the  nature  of  the 
disease  is  essentially  progressive,  and  at  the  end  of  from  two  to  six 
years  the  second  stage  of  the  disease  is  constituted  by  the  appearance 
of  marked  and  persistent  paralysis  with  contractures.  During  the 
second  stage,  which  lasts  from  four  to  six  years  or  more,  the  nervous 
symptoms  remain  more  or  less  stationary,  and  the  general  nutrition  is 
but  little  impaired.  In  the  third  stage  of  the  disease  the  patient  loses 
his  appetite  and  becomes  emaciated,  the  bladder  is  paralyzed,  cystitis 
and  bedsores  appear,  and  the  patient  dies  from  septic  fever.  In  other 
cases  death  is  caused  by  a  bulbar  paralysis,  or  by  some  intercurrent 
disease  like  pneumonia,  pleurisy,  or  phthisis. 


Ill,  CHOREA. 

Etiology. — Heredity  plays  an  important  part  in  the  production  of 
chorea,  but  the  transmission  is  probably  always  indirect.  The  disease 
chiefly  attacks  children,  often  occurring  about  puberty,  although  chil- 
dren at  the  breast  and  young  women  are  sometimes  attacked.  Girls 
are  much  more  frequently  affected  than  boys.  Everything  which  aug- 
ments the  excitability  of  the  nervous  system  during  the  period  of  sexual 
develoimient,  such  as  premature  excitement  of  the  sexual  passion,  onan- 
ism, or  any  undue  emotional  disturbance,  increases   the  tendency  to 


680  CHOREA. 

chorea.  But  the  most  usual  predisposing  causes  in  adults  are  preg- 
nancy and  menstrual  disorders,  and  chlorosis.  That  some  causal  rela- 
tionship exists  between  articular  rheumatism  and  chorea  has  been  known 
since  the  beginning  of  the  century,  but  the  true  nature  of  this  relation- 
ship is  not  yet  accurately  ascertained.  Out  of  two  hundred  and  four- 
teen cases  of  chorea  analyzed  by  Dr.  Moury,  thirty-three  had  suffered 
from  rheumatic  fever  and  twenty-three  from  rheumatic  jjains,  while  in 
nine  cases  the  history  of  rheumatism  was  very  doubtful,  tliese  figures 
o-iving  from  twenty-nine  to  thirty-two  per  cent,  of  cases  in  which  a 
rheumatic  history  could  be  traced.  Chorea  occurs  frequently  after 
scarlet  fever,  a  fact  which  may  probably  be  explained  by  the  frequency 
with  which  scarlet  fever  is  followed  by  rheumatism.  Chorea  sometimes 
occurs  during  pregnancy.  It  is  mt>st  frequent  during  first  pregnancy, 
but  it  is  sometimes  repeated  in  the  same  patient  in  subsequent  pregnan- 
cies. It  appears  more  frequently  during  the  first  than  the  second  half 
of  pregnancy,  but  it  sometimes  begins  in  the  later  months,  and  may 
continue  up  to  the  time  of  delivery  or  beyond  it.  The  majority  of 
those  affected  are  from  twenty  to  thirty  years  of  age.  The  disease  is 
more  prevalent  in  large  cities  tlian  in  the  country,  and  race  appears  to 
influence  the  production  of  the  disease,  inasmucli  as  in  South  America 
the  black  is  much  less  frequently  attacked  than  the  white  population. 
Of  the  exciting  causes  of  cliorea,  the  most  frecjuent  and  important  are 
emotional  disturbances,  such  as  fright,  sorrow,  and  discontent.  Hys- 
terical girls  and  those  who  are  strongly  predisposed  to  chorea,  or  wlio 
have  already  suffered  from  an  attack,  may  acquire  the  disease  from 
imitation  of  others  suffering  from  it. 

Symptoms. — The  development  of  tlie  characteristic  phenomena  of 
chorea  is  generally  preceded  for  a  variable  period  of  days  or  weeks  by 
various  premonitory  symptoms.  The  most  usual  of  these  are  afforded 
by  changes  in  the  character  and  disposition  of  the  patient,  who  becomes 
forgetful,  inattentive,  fretful,  and  discontented  or  apathetic,  while  the 
intellectual  powers  are  impaired.  The  irregular  spasmodic  muscular 
contractions  of  chorea  are  not  unfrequently  ushered  in  by  a  slight 
dragging  of  one  of  tlie  lower  extremities,  with  a  tendency  to  walk  in  a 
curved  line  and  liability  to  let  objects  fall  from  the  hand.  Tbese  mani- 
festations of  the  approaching  disease  are  probably  due,  in  some  degree, 
to  irregular  muscular  contractions,  but  are  largely  dependent  upon 
muscular  weakness,  and  in  some  cases  paralysis  may  be  so  pronounced 
that  the  case  may  be  mistaken  for  hemiplegia.  The  characteristic 
choreic  movements  generally  begin  in  the  small  muscles  of  the  face  and 
in  those  of  a  hand.  They  consist  at  first  of  grimaces  and  other  con- 
tortions of  the  face,  and  slight  jerking  movements  of  the  fingers  and  at 


SYMPTOMS.  681 

the  wrist-joint,  with  pronation  of  the  forearm,  Avhen  the  patient  is  con- 
scious of  being  observed  or  is  excited  from  any  other  cause ;  these  soon 
increase  in  intensity  and  persist  during  repose. 

The  irreguLar  contractions  soon  extend  so  as  to  involve  all  the  voluntary 
muscles,  when  the  affection  may  be  called  f/eneral  chorea,  or  they  remain 
more  or  less  limited  to  the  muscles  of  one-half  of  the  body,  when  the 
disease  is  called  unilateral  chorea  or  hemichorea. 

G-eneral  Chorea. — When  once  the  disease  is  fully  established  the 
symptoms  are  quite  characteristic,  and  it  would  be  difficult  to  find 
phrases  more  expressive  of  the  disorderly  muscular  movements  than 
'•  insanity  of  the  muscles,"  adopted  by  Bellingham,  and  "  folic  muscu- 
laire"  by  Bouillaud. 

The  features  undergo  every  variety  of  contortion.  The  brow  is  knit 
and  immediately  expanded ;  the  eyebrows  are  elevated  and  the  next 
moment  depressed,  or  one  may  be  elevated  while  the  other  is  lowered  ; 
the  eyelids  open  and  close  alternately ;  the  eyeballs  are  quickly  rotated 
in  different  directions ;  and  the  labial  commissures  are  suddenly  drawn 
outwards,  and  as  quickly  retracted.  These  opposite  movements  succeed 
one  another  with  such  rapidity  that  the  fiice  presents  in  quick  succession 
the  most  contradictory  expressions,  such  as  those  of  delight,  vexation, 
and  anger. 

The  tongue  is  thrust  out  of  the  mouth,  and  quickly  retracted  and 
rolled  about  from  side  to  side  ;  the  jaws  are  separated  and  closed,  it  may 
be  with  so  much  violence  that  teeth  are  broken,  or  the  tongue  and  cheeks 
are  severely  bitten  ;  lateral  displacements  of  the  lower  jaw  are  frequently 
observed,  and  the  head  is  jerked  suddenly  from  one  side  to  the  other, 
while  the  facial  grimaces  by  which  the  movements  of  the  jaws,  tongue, 
and  head  are  accompanied  add  to  the  comical  appearance  presented  by 
the  patient.  The  pupils  are  usually  dilated  and  their  reaction  to  light 
is  diminished. 

The  superior  extremities  execute  every  variety  of  movement,  the 
shoulders  are  elevated,  then  lowered,  and  immediately  afterwards  drawn 
backwards  or  forwards  ;  the  arm  and  forearm  are  moved  at  the  shoulder- 
and  elbow-joint  in  every  possible  direction  ;  the  hand  is  alternately  pro- 
nated  and  supinated,  flexed  and  extended  ;  and  the  fingers  are  at  one 
moment  extended  and  spread  apart  and  at  the  next  flexed.  These 
movements  are  combined  in  such  varied  ways  that  a  gesticulatory  agita- 
tion is  produced  which  defies  description. 

The  muscles  of  the  trunk  are  implicated,  and  their  unequal  disorderly 
contractions  produce  sudden  lateral  and  antero-posterior  deviations  of 
the  vertebral  column,  which  in  certain  cases  may  be  so  violent  that 
the  patient  is  thrown  from  his  chair  or  out  of  bed.     The  muscles  of  the 


682  CHOREA. 

lower  extremities  also  undergo  irregular  contractions,  causing  eversion 
and  inversion  of  the  foot  and  various  contortions  of  the  toes,  as  well  as 
movements  at  the  larger  articulations.  The  respiratory  j-hvthm  becomes 
irregular  and  jerky,  and  on  laryngoscopic  examination  the  vocal  cords 
have  been  observed  to  act  in  an  irregular  and  disorderly  manner. 

Choreic  movements  may  persist  during  repose,  and  are  much  ex- 
aggerated during  voluntary  effort  and  when  the  patient  is  under  obser- 
vation or  excited  in  any  way,  but  they  cease  during  sleep,  and  also 
under  the  influence  of  chloroform,  in  all  but  very  aggravated  cases.  In 
cases  of  moderate  intensity  delicate  manual  operations,  such  as  those 
required  for  writing,  sewing,  and  playing  upon  musical  instruments, 
become  alone  impossible ;  while  operations,  like  eating,  requiring  less 
complicated  adjustments  for  their  performance,  are  still  effected,  although 
in  an  imperfect  and  roundabout  manner,  and  after  frequent  interrup- 
tions from  the  involuntary  contraction  of  antagonistic  muscles. 

In  aggravated  cases  it  becomes  impossible  to  execute  almost  any  in- 
tended movement.  When  the  patient  endeavors  to  carry  anything  to 
his  mouth,  such  as  a  glass  of  water,  the  progress  of  his  arm  is  arrested 
by  a  series  of  jerks  and  contradictory  movements  which  may  scatter 
the  contents  of  the  glass  in  every  direction ;  the  patient  cannot  button 
or  unbutton  his  clothes ;  the  maintenance  of  the  erect  posture  is 
difficult  or  impossible;  and  even  in  the  recumbent  posture  he  is  not 
free  from  the  danger  of  being  thrust  out  of  bed ;  his  clothes  and  linen 
become  worn  out  by  constant  rubbing;  and  the  skin  over  the  prominent 
bones  becomes  erythematous  and  may  ulcerate. 

On  the  patient's  being  asked  to  show  the  tongue,  he  protrudes  it  with 
a  jerk,  the  mouth  being  opened  to  an  unnecessary  extent;  the  tongue 
is  immediately  withdrawn,  while  the  mouth  and  jaws  close  upon  it  with 
violence.  When  the  patient  endeavors  to  speak,  the  convulsive  action 
of  the  facial  muscles  becomes  aggravated ;  his  articulation  is  irregular, 
jerky,  drawling,  or  stammering;  his  voice  is  monotonous;  and  in 
aggravated  cases  his  speech  is  so  disordered  as  to  be  almost  if  not 
entirely  unintelligible.  Spasmodic  contraction  extends  to  the  muscles 
of  mastication  and  deglutition,  and  consequently  these  functions  are 
performed  imperfectly  and  with  difficulty, 

Hemichorea. — The  spasmodic  phenomena  are  sometimes  limited  to 
the  muscles  of  one-half  the  body,  the  unilateral  variety  occurring  in 
about  one-fifth  of  all  cases.  Disorders  of  speech  are  usually  more 
marked  when  the  right  than  when  the  left  side  is  affected  with  spasm, 
although  speech  is  sometimes  disordered  Avhen  the  left  side  is  solely 
affected.  Broadbent  asserts  that  the  muscles  bilaterally  associated  in 
their  actions,  and  which  are  comparatively  spared  in  hemiplegia,  are 


SYMPTOMS.  683 

aftected  to  some  extent  on  both  sides  in  liemichorea.  The  other  symp- 
toms of  hemichorea  are  the  same  as  those  of  general  chorea,  and  do  not 
require  separate  description. 

Although  spasmodic  motor  disturbance  constitutes  the  most  charac- 
teristic feature  of  chorea,  it  must  not  be  forgotten  that  a  certain  decree 
of  muscular  weakness  is  always  present,  this  being  easy  of  recognition 
in  cases  of  hemichorea.  Indeed,  towards  the  termination  of  the  affec- 
tion or  during  its  course,  the  choreic  movements  may  be  replaced  by  a 
more  or  less  complete  hemiplegia  or  paraplegia,  and  we  have  already 
seen  that  paralytic  symptoms  may  precede  the  development  of  the  char- 
acteristic movements. 

The  electric  excitability  of  the  nerves  and  muscles  is  said  to  be  in- 
creased to  both  currents,  a  fact  more  readily  proved  in  hemichorea  than 
in  the  bilateral  variety. 

The  reflex  excitability  is  said  by  some  authors  to  be  increased  and 
by  others  to  be  diminished. 

Sensory  disturbances  are  not  frequently  observed  in  chorea.  Painful 
points  have  been  found  at  times  in  the  course  of  the  nerve  trunks  of 
the  affected  region,  while  tenderness  on  pressure  over  the  spinous  pro- 
cesses of  some  of  the  vertebrae  is  occasionally  met  with.  At  other  times 
cutaneous  hyperaesthesia  or  hyperalgesia  distributed  over  half  or  the 
whole  of  the  body  has  been  observed,  but  anfesthesia  of  like  distribution 
is  more  common, 

Vaso-motor  and  secretory  disturbances  are  wanting,  there  are  no 
special  trophic  changes,  and  the  general  health  does  not  suffer,  except 
in  aggravated  and  chronic  cases,  in  which  the  constant  agitation  and 
want  of  sleep  induce  a  condition  of  angemia  and  general  marasmus. 

Psychical  disturbances  are  invariably  observed  in  chorea.  The 
mental  depression  and  irritability  with  which  the  disease  begins  usually 
increase  during  its  course.  The  patient  is  obstinate,  taciturn,  and  even 
violent  towards  parents  and  attendants.  He  suffers  from  impairment  of 
memory,  incapacity  for  thinking,  and  general  intellectual  weakness. 
At  times  there  may  be  hallucinations  of  sight,  especially  at  night,  suc- 
ceeded by  a  maniacal  delirium,  and  according  to  the  observations  of 
Marce,  half  of  the  cases  in  which  this  delirium  supervenes  terminate 
fatally. 

The  pulse  may  be  irregular,  and  the  patient  suffers  from  palpitation, 
while  a  physical  examination  of  the  heart  generally  reveals  the  presence 
of  endocardial  murmurs,  either  arising  from  disease  of  the  valves  or  of 
functional  origin.  Chorea  is  not  usually  accompanied  by  pyrexia,  but 
in  severe  cases,  when  there  is  violent  muscular  action,  elevation  of  tem- 


684 


CHOKEA, 


perature  is  not  uncommon.  When  chorea  is  associated  Avith  acute  rheu- 
matism more  or  less  fever  is  necessarily  present. 

Chorea  usually  runs  a  chronic  course,  the  majority  of  cases  lasting 
from  six  to  eight  weeks,  and  aggravated  cases  four  to  five  months. 
Chorea  frequently  recurs,  a  fresh  attack  being  excited  by  a  slight  emo- 
tional disturbance,  pregnancy,  or  the  presence  of  an  acute  disease. 
Chorea  usually  terminates  in  complete  recovery.  The  disease  is  not 
often  fatal  in  children,  but  a  fiital  termination  may  occur  from  a  com- 
plication of  rheumatism  and  endocarditis,  or  from  cerebral  symptoms, 
consisting  of  collapse  with  complete  muscular  relaxation  and  involuntary 
evacuations,  and  a  final  coma. 

Morbid  Anatomy. — Post-mortem  investigation  has  not  thrown  much 
light  upon  the  nature  of  paralysis  agitans.  The  chief  changes  which 
have  been  discovered  consist  of  obliteration  of  the  central  canal  of  the 
spinal  cord  from  increase  of  the  epithelium  of  the  ependyma,  and  pig- 
mentation of  the  <2;ano;lion  cells  of  the  column  of  Clarke,  anterior  horns, 
olivary  body,  and  corpus  dentatum  of  the  cerebellum.  Slight  evidences 
of  sclerosis  were  found  in  the  lateral  columns  of  the  cord  as  well  as  in 
the  corpora  striata  and  the  hemispheres  of  the  brain. 

Multiple  sclerosis  consists  of  a  chronic  infiammation  which  appears 
in    well-defined   nodules,    and    is   widely    distributed    throughout    the 

Fi<».  181. 


Section  ok  the  Anterior  Oray  Horn  of  the  Cervical  Enlargement  of  the  Spinal  Cord  from  a 

Case  of  Chorea  that  died  on  the  Foirtii  Day  of  Scarlet  Fever.     (Bury.) 

cc,  Otntral  canal  ;  nc,  Anterior  commissure  ;  A,  Anterior  horn. 

nervous  system.  In  the  spinal  cord  these  nodules  vary  from  the  size 
of  a  hemp  seed  to  that  of  a  bean,  but  they  often  become  confluent  and 
appear  to  attain   a  much  larger  size  in   the  brain.     On  section   the 


MO  K  BID    ANATOMY. 


685 


nodules  appear  gray  or  grayish-yellow,  and  when  exposed  to  the  air 
change  to  a  salmon  color ;  they  are  translucent  or  opaque,  irregular  or 
oval  in  shape,  generally  isolated  and  circumscribed,  but  occasionally 
confluent,  and  are  in  consistence  dense,  tough,  even  cartilaginous,  but 
on  rare  occasions  semifluid  and  gelatinous.  The  distribution  of  the 
nodules  is  very  variable.  On  making  successive  transverse  sections  of 
the  cord  the  nodules  will  appear  in  one  or  both  the  lateral  columns  at 
one  level,  in  the  posterior  columns  at  another,  in  the  gray  substance  at 
a  third,  and  in  the  whole  transverse  area  of  the  cord  at  a  fourth.     The 


Fig.  182. 


Section  of  the  Cervical  Region  of  the  Spinal  Cord  from  a  Case  of  Chorea.     (Young  ) 
cc,  Central  canal  ;  A  and  P,  Anterior  and  Posterior  horns  respectively. 

fjivorite  sites  in  the  cerebral  hemispheres  are  the  Avhite  substance  of  the 
centrum  ovale,  the  septum  lucidum,  the  corpus  callosum,  the  basal  gan- 
glia, and  the  walls  of  the  lateral  ventricles.  In  the  cerebellum  the 
nodules  are  generally  found  in  the  white  substance.  The  cortices  of 
the  cerebellum  and  cerebrum  are  singularly  free  from  nodules.  The 
anterior  and  posterior  roots  of  the  spinal  nerves  have  been  found  dis- 
eased, and  the  cranial  nerves,  in  tlieir  passage  along  the  base  of  the 
skull,  are  particularly  liable  to  be  affected.  The  number  of  nodules 
which  are  present  in  one  case  is  very  variable,  a  few  only  being  ob- 
served in  some  cases,  while  in  others  hundreds  may  be  counted*. 

In  most  fatal  cases  of  chorea  which  have  been  examined  after  death, 
small  fibrinous  vegetations  have  been  found  studded  along  the  edges  of 


686  CHOREA. 

the  mitral  valve.  Various  changes  have  been  described  by  different 
observers  as  having  been  met  with  in  the  nervous  system.  These 
changes,  according-  to  Dr.  Dickinson,  consist  of  dilatation  of  the  medium 
sized  arteries  and  veins  throughout  the  substance  of  the  brain  and 
spinal  cord,  exudation,  small  hemorrhages,  and  patches  of  necrotic 
softening,  or,  in  chronic  cases,  of  sclerosis  in  the  neighborhood  of  the 
vessels.  These  changes  were  more  pronounced  in  the  corpora  striata, 
optic  thalami,  the  anterior  perforated  spaces,  and  at  the  junction  of 
the  posterior  gray  horns  and  central  column  of  the  spinal  cord  (Fig. 
181).  In  a  fatal  case  of  chorea  examined  by  myself,  all  the  vessels 
of  the  spinal  cord  were  found  more  or  less  distended  with  red  blood- 
corpuscles,  and  in  some  sections  a  fibrinous  plug,  which  distended 
the  vessel,  was  observed  in  the  anterior  or  antero-lateral  arteries 
(Fig.  182).  Spots  of  necrotic  softening  were  also  observed  in  the 
basal  ganglia. 

3Iorhid  Physiology. — The  tremors  of  paralysis  agitans  are  most 
probably  caused  by  a  loss  of  the  balance  normally  existing  between  the 
regulative  functions  of  the  cerebrum  and  cerebellum.  The  attitude  of 
paralysis  agitans  is,  as  lias  been  pointed  out  by  Dr.  Hughlings-Jackson, 
the  opposite  of  that  of  tetanus.  During  a  tetanic  seizure  the  action  of 
the  extensors  of  the  trunk  and  lower  extremities  predominates,  and  the 
body  is  arched  backwards  ;  iji  paralysis  agitans  the  action  of  the  flexors 
predominates,  so  that  the  dift'erent  segments  of  the  trunk  and  extremi- 
ties are  flexed  upon  one  another.  In  tetanus  the  muscles,  the  actions 
of  which  must  have  gradually  prcdominateil  in  the  course  of  evolution 
so  as  to  attain  the  erect  posture,  are  excited  to  increased  activity, 
while  in  paralysis  agitans  the  same  muscles,  speaking  broadly,  become 
relatively  paralyzed,  and  there  is  a  gradual  reduction  of  the  human  to 
the  animal  posture.  In  the  stage  of  propulsion  the  attitude  of  the 
patient  is  very  similar  to  that  of  a  dog  attempting  to  walk  on  his  hind 
legs.  The  phenomena  of  propulsion  are  caused  partly  by  the  forced 
attitude  of  the  patient  and  partly  by  the  great  slowness  with  which  his 
movements  are  executed.  When  once  the  heel  is  raised  from  the 
ground  by  contraction  of  the  muscles  of  the  calf,  the  patient  on  getting 
up  must  balance  himself  on  his  toes,  but  in  walking  the  forward  in- 
clination of  the  body  tends  to  make  the  line  of  gravity  pass  in  front  of 
the  active  leg.  The  position  is  to  some  extent  the  same  as  that  assumed 
by  a  person  in  running.  But  a  healthy  runner  is  able  to  take  rapid 
and  long  strides  with  the  passive  leg,  and  by  the  time  it  is  brought  to 
the  ground  it  is  well  in  advance  ef  the  line  of  gravity,  and  the  body  is 
thus  kept  from  falling. 

In  paralysis  agitans,  however,  the  rigidity  of  the  muscles  prevents 


MORBID    PHYSIOLOGY.  687 

the  patient  from  taking  a  long  j^tride,  and  the  slowness  with  which  the 
movements  are  executed  renders  it  impossible  for  him  to  plant  the  leo- 
that  is  about  to  become  active  in  front  of  the  line  of  gravity,  and  con- 
sequently the  patient  tends  to  fall  forwards  at  every  step.  In  retropul- 
sion  the  line  of  gravity  ever  tends  to  fall  behind  the  ball  of  the  toe  of 
the  active  leg,  and  the  other  leg  cannot  be  moved  backwards  with  suffi- 
cient celerity  to  enable  the  patient  to  place  it  far  enough  behind  the 
retreating  centre  of  gravity  in-order  to  ari-est  the  backward  movement. 
It  is  difficult  to  connect  the  chief  symptoms  of  paralysis  agitans  with 
the  morbid  changes  which  have  been  discovered  after  death,  but  it  must 
be  remembered  that  these  changes  are  not  limited  to  the  spinal  cord, 
but  are  widely  diffused  over  the  encephalo-spinal  centres  and  conduct- 
ing paths.  There  is  at  least  nothing  in  the  changes  which  have  been 
discovered  after  death  incompatible  with  the  idea  that  paralysis  agitans 
is  a  dissolution  of  those  nervous  mechanisms  whose  action  must  have 
gradually  predominated  in  passing  from  the  quadrupedal  position  of 
animals  to  the  bipedal  position  of  man. 

In  multiple  sclerosis  the  nodules  are  widely  distributed  over  different 
parts  of  the  nervous  system,  and  the  implication  of  different  parts  of  the 
nervous  system,  having  different  functions,  affords  a  ready  explanation 
of  the  chief  symptoms  of  the  disease.  Implication  of  the  lateral  columns 
explains  the  paresis,  contractures,  excess  of  the  tendon-reflexes,  and  the 
phenomena  grouped  under  the  name  of  spinal  epilepsy,  of  the  posterior 
columns,  the  ataxia;  of  the  anterior  horns,  the  muscular  atrophy;  and 
of  the  bulbar  nuclei,  the  labio-glosso-pharyngeal  paralysis  which  may 
be  present  in  different  cases,  while  the  student  who  is  tolerably  w^ell  ac- 
quainted with  the  physiology  of  the  nervous  system  will  be  able  to  con- 
nect the  remaining  symptoms  with  the  appearance  of  those  nodules  in 
different  parts  of  the  cerebrum,  cerebellum,  pons,  and  crura.  Charcot 
attributes  the  characteristic  tremor  of  multiple  sclerosis  to  the  long  per- 
sistence of  the  axis-cylinders  in  the  nodules  of  sclerosis.  Conduction  will 
take  place  through  the  nerve  fibres  long  after  they  are  involved  in  the 
nodules  of  the  disease,  but  when  once  the  medullary  sheath  is  destroyed 
the  conduction  will  be  so  retarded  that  the  impulses  from  the  cortex  do 
not  pass  in  a  sufficiently  quick  succession  to  cause  a  continuous  con- 
traction. It  has,  however,  been  pointed  out  by  Erb,  that  the  charac- 
teristic tremors  are  absent  in  purely  spinal  cases,  and  that  in  all  cases 
in  which  tremors  were  present  during  life  nodules  were  discovered  after 
death  in  the  medulla  oblongata,  pons,  crura  cerebri,  and  other  parts  of 
the  brain.  It  Avould  seem,  therefore,  that  in  this  disease  again  the 
tremors  are  caused  by  a  loss  of  balance  between  the  regulative  functions 
of  the  cerebrum  and  cerebellum. 


688  CHOREA. 

In  chorea  the  lesions  are  supposed,  by  Broadbent  and  Hughlings-Jack- 
son,  to  be  localized  in  the  corpus  striatum,  optic  thalamus,  and  cortex  of 
the  brain,  but  they  are  still  more  widely  distributed  over  the  nervous 
system.  It  was  first  suggested  by  Kirkes  that  chorea  is  caused  by  mul- 
tiple embolism  of  the  vessels  of  the  brain  and  spinal  cord,  produced  by 
fibrinous  particles  being  Avashed  off  from  the  valves  of  the  heart  after 
endocarditis.  This  theory,  which  has  been  elaborated  by  Dr.  Hughlings- 
Jackson  and  others,  has  many  facts  in  its  favor,  and  now  there  can 
scarcely  be  a  doubt  that  chorea  is  often  caused  by  multiple  embolism. 
Choreiform  movements  have,  indeed,  been  produced  in  animals  by  Dr. 
Angel  Money,  by  injecting  inert  powders  into  the  circulation.  At  the 
same  time,  it  must  be  remembered  that  chorea  may  occur  in  persons  who 
are  free  from  suspicion  of  a  cardiac  complication,  and  it  seems  likely, 
therefore,  that  the  affection  may  be  caused  by  other  conditions  besides 
multiple  embolism.  It  seems  likely,  indeed,  that  the  symptoms  of 
chorea  may  be  caused  in  the  cliildren  of  neuropathic  families  by  condi- 
tions which  lower  the  nutrition  of  the  nervous  system. 

Treatment. — Paralysis  agitans  being  a  progressive  disease,  its  treat- 
ment can  only  be  palliative.  The  internal  remedies  which  have  been 
used  are  carbonate  of  iron,  chloride  of  barium,  hyoscyamus,  strychnine, 
ergot,  belladonna,  quinine,  zinc,  nitrate  of  silver,  chloride  of  gold, 
arsenic,  and  phosphorus,  and  of  these  probably  the  last  two  are  the 
most  deserving  of  trial.  Morj)hia  and  other  narcotics  are  necessary 
adjuncts  of  treatment  in  the  later  stages  of  the  disease,  when  the  patient 
is  harassed  by  restlessness  and  sleeplessness,  and  both  chloral  and 
bromide  of  potassium  may  then  be  of  use. 

Multiple  sclerosis  must  be  treated  on  the  same  general  principles  as 
chronic  myelitis.  The  most  promising  method  of  treatment  appears  to 
be  the  persistent  application  of  the  galvanic  current  to  tlie  spine,  hydro- 
pathy, nitrate  of  silver,  phosphorus,  cod-liver  oil,  and  nourishing  but 
unstimulating  diet.  The  greatest  improvement  that  I  ever  saw  take 
place  in  this  disease  was  in  the  case  of  a  man  who,  acting  on  my  advice, 
changed  the  sedentary  occupation  of  a  clerk  in  a  factory  for  that  of  a 
farmer. 

Ohorea  should  be  treated  by  the  careful  regulation  of  the  diet,  and 
by  the  removal  of  every  source  of  reflex  irritation,  such  as  intestinal 
worms.  If  anaemia  be  present,  iron  may  be  given,  and  if  rheumatism 
complicates  the  case,  salicylate  of  sodium  must  be  administered,  while  the 
hot  vapor  bath  may  be  of  service.  The  child  should  in  all  cases  be 
removed  from  school,  and  all  intellectual  work  ought  to  be  suspended. 
Of  internal  remedies,  arsenic  and  zinc  are  the  most  useful.  Arsenic  is 
best  given   in  the  form  of  the  ordinary  liquor  arsenicalis,  and  of  this 


MORBID    PHYSIOLOGY.  689 

preparation  the  dose  should  be  from  two  to  five  minims  gradually  in- 
creased up  to  from  five  to  ten  minims  three  times  a  day,  according  to 
the  age  of  the  patient.  The  sulphate  is  the  most  convenient  salt  of 
zinc  to  employ.  A  dose  of  two  or  three  grains  may  be  given  at  first, 
three  times  a  day,  and  the.  dose  should  be  gradually  increased  daily  until 
the  almost  incredibly  large  quantity  of  from  fifteen  to  twenty  grains  is 
taken  three  times  a  day.  If  nausea  or  vomiting  is  produced,  the  dose 
should  be  slightly  diminished  for  a  few  days  until  tolerance  is  established. 
Bromide  of  potassium  or  chloral  hydrate  are  useful  when  psychical  dis- 
turbances and  sleeplessness  are  prominent  symptoms,  but  they  do  not 
appear  to  exercise  a  decided  influence  on  the  course  of  the  disease.  At 
the  Cheadle  Convalescent  Hospital  Dr.  Wausburgh  Jones  is  having 
marked  success  in  the  treatment  of  chorea,  by  rest  in  bed,  seclusion, 
overfeeding,  and  massage,  or  by  the  S.  Weir-Mitchell  treatment. 


44 


CHAPTEK    XXI. 

GENERAL  DIAGNOSIS. 

Before  brinerino;  the  work  to  a  close,  it  will  be  desirable  to  make  a 
few  remarks  on  diagnosis,  and  although  much  of  what  we  shall  have  to 
say  will  be  a  mere  repetition,  yet  it  will  prove  useful  to  discuss  the 
general  principles  of  this  important  subject  disencumbered  from  the 
details  of  clinical  descriptions.  The  diagnosis  of  the  diseases  of  the 
nervous  system  may  be  divided  into:  1,  the  clinical;  2,  the  topo- 
graphical; and  3,  the  pathological  diagnosis. 

1.  CLINICAL  DIAGNOSIS. 

With  the  view  of  arriving  at  a  satisfactory  clinical  diagnosis,  which 
must  form  the  basis  of  the  other  kinds  of  diagnosis,  the  patient  must  be 
subjected  to  a  methodical  examination.  The  various  tests  which  have 
already  been  described  must  be  systematically  aj)plied  in  order  to  dis- 
cover the  sensory,  motor,  vaso-motor,  trophic,  and  psychical  disturbances 
which  may  be  present.  At  the  end  of  the  examination  the  observations 
which  have  been  made  are  systematized,  when  it  is  concluded  that  the 
patient  is  suifering  from  local  anfesthesia,  paranesthesia,  hemianaes- 
thesia,  local  spasms,  monospasms,  unilateral  convulsions,  general  con- 
vulsions, atrophic  paralysis,  spasmodic  paralysis,  jiaraplegia,  hemiplegia, 
and  monoplegia,  either  separately  or  in  various  combinations.  It  should 
also  be  noted  whether  the  disease  is,  in  its  mode  of  onset,  fulminant,  acute, 
or  chronic,  and  its  origin  idiopathic,  traumatic,  syphilitic,  or  arises  from 
any  other  cause.  Our  knowledge  of  many  diseases  is,  indeed,  so  slender 
that  they  admit  of  only  a  clinical  diagnosis.  When,  for  example, 
general  convulsions  occur  at  irregular  intervals  and  in  association  with 
various  emotional  manifestations,  we  call  them  hysteria  ;  when  they  recur 
at  regular  intervals  in  the  absence  of  such  manifestations,  we  call  them 
epilepsy ;  when  they  occur  as  an  acute  affection  without  showing  a 
tendency  to  periodical  recurrence,  we  call  them  eclampsia,  these  being 
subdivided  according  to  the  cause  of  the  symptoms  into  toxic,  puerperal, 
uraemic,  febrile,  and  reflex  convulsions  ;  and  when  no  cause  for  them 
can  be  assigned,  we  call  them  idiopathic  convulsions. 


TOPOGRAPHICAL    DIAGNOSIS.  691 

2.  TOPOGRAPHICAL  DIAGNOSIS. 

In  a  large  number  of  cases  we  are  enabled  to  pass  readily  from  the 
clinical  to  the  topographical  diagnosis.  In  order  to  determine  the 
locality  of  the  lesion,  it  is  all  important  to  remember  the  course  of  the 
sensory  conducting  paths  from  the  periphery  up  to  their  termination  in 
the  sensory  centres  of  the  cortex  of  the  brain,  and  of  the  motor  con- 
ducting paths  from  their  origin  in  the  motor  centres  of  the  cortex  to 
their  termination,  first  in  the  spinal  nuclei  and  then  in  the  various 
muscles.  In  reference  to  the  sensory  symptoms,  it  may  be  said  that 
when  the  disorder  is  more  or  less  limited  to  the  area  of  distribution  of 
the  afferent  branches  of  a  particular  nerve  the  lesion  is  situated  in  the 
peripheral  course  of  the  nerve,  when  it  is  distributed  pretty  uniformly 
over  the  lower  half  of  the  body  and  the  lower  extremities  the  lesion  is 
situated  in  the  spinal  cord,  and  when  it  is  distributed  over  one  lateral 
half  of  the  body  the  lesion  is  situated  in  the  brain,  the  posterior  third 
of  the  posterior  segment  of  the  internal  capsule  being  the  part  usually 
affected.  Similar  remarks  apply  to  the  motor  symptoms.  When  a 
paralysis,  for  example,  is  limited  to  the  muscles  supplied  by  the 
branches  of  a  particular  nerve,  the  lesion  is  likely  to  be  situated  in  the 
peripheral  course  of  the  nerve;  when  the  paralysis  is  pretty  uniformly 
distributed  over  the  lower  half  of  the  body  the  lesion  is  situated  in. 
the  spinal  cord,  and  when  it  is  restricted  to  a  lateral  half  of  the  body 
the  lesion  is  localized  in  the  brain.  The  division  of  the  various  forms 
of  loss  of  motor  power  into  atrophic  and  spasmodic  paralyses  is  a  most 
important  one  for  diagnostic  purposes.  In  atrophic  paralysis  the  lesion 
is  situated  in  the  anterior  gray  horns  of  the  spinal  cord,  in  the  fibres 
which  connect  the  ganglion  cells  of  these  horns  with  the  muscles,  or  in 
the  affected  muscles  themselves.  In  the  spasmodic  paralyses  the  lesion 
is  situated  in  the  motor  centres  of  the  cortex  or  in  the  conducting 
paths  which  connect  these  centres  with  the  motor  ganglion  cells  of  the 
anterior  gray  horns  of  the  spinal  cord.  Loss  of  the  reflexes  indicates, 
as  a  rule,  that  the  lesion  is  situated  in  the  spinal  reflex  loops,  Avhile 
excess  of  them  generally  shows  that  it  is  situated  in  the  motor  centres 
of  the  cortex,  or  in  the  conducting  paths  which  connect  these  with  the 
spinal  nuclei.  General  symptoms  like  headache,  vomiting,  optic 
neuritis,  incoherence,  delirium,  and  loss  of  consciousness,  indicate  that 
the  brain  is  implicated,  but  they  are  of  no  further  value  in  locahzing 
the  disease.  Before  proceeding  further  with  our  subject,  it  will  be  well 
to  mention  some  general  difficulties  which  present  themselves  in  local- 
izing the  lesion.     The  first  is  that  the  degree  of  the  symptoms  does  not 


692  GENERAL    DIAGNOSIS. 

by  any  means  always  correspond  to  the  size  and  extent  of  the  lesion. 
A  hemorrhage  may,  by  suddenly  rupturing  some  of  the  fibres  of  the 
conducting  paths  and  compressing  others,  give  rise  to  sensory  and 
motor  disorders  out  of  proportion  to  the  extent  of  the  lesion,  while  a 
slow  growing  tumor  may,  by  gradually  displacing  and  stretching  the 
fibres  of  the  conducting  paths,  come  to  occupy  the  usual  situation  of 
these  paths  without  causing  but  a  slight  degree  of  motor  or  sensory 
disorder.  It  may,  indeed,  be  laid  down  as  a  general  rule  that  acute 
lesions  are  often  much  smaller,  and  chronic  lesions  much  larger  than 
the  degree  and  character  of  the  symptoms  would  lead  us  to  expect. 
The  second  difficulty  is  that  a  lesion  not  only  causes  direct  symptoms 
from  irritation  or  destruction  of  the  nervous  tissues  in  its  immediate 
vicinity,  but  often  produces  marked  indirect  symptoms  by  excitation  or 
inhibition  of  remote  parts,  Goltz,  for  example,  found  that  section  of 
the  spinal  cord  in  the  cervical  region  in  dogs  causes  immediate  paralysis 
of  the  power  of  erection  of  the  penis,  but  if  the  animal  survive  for  a 
few  days  this  function  recovers,  and  an  erection  may  be  obtained  by 
reflex  excitation.  Indirect  symptoms,  having  a  similar  import,  are  fre- 
quently met  with  in  disease,  and  this  is  particularly  apt  to  be  the  case 
when  the  lesion  is  situated  in  the  brain.  A  small  irritative  lesion, 
when  situated  in  the  cortex  of  the  brain,  may  set  up  widely  diffused 
discharges,  and  thus  give  rise  to  extensive  unilateral  spasms  or  even  to 
general  convulsions.  A  small  hemorrhage  in  the  substance  of  the 
brain  may,  partly  through  the  shock  communicated  to  the  whole  organ 
from  the  suddenness  of  the  onset,  and  partly  from  the  compression  it 
exercises  upon  the  nervous  tissues  by  encroaching  upon  the  volume  of 
the  cranial  cavity,  suddenly  arrest  all  the  functions  of  the  organ,  so 
that  the  patient  lies  in  an  unconscious  condition,  and  with  almost  com- 
plete muscular  relaxation.  When  the  indirect  symptoms  are  so  pre- 
dominant as  in  the  example  just  given,  it  will  not  be  found  possible  to 
recognize  the  direct  symptoms  or  to  interpret  their  significance.  But 
in  most  cases  the  indirect  symptoms  tend  to  pass  off  in  a  few  days,  and 
then  the  localization  of  the  lesion  may  be  detemiined.  Having  come 
to  the  conclusion  that  the  lesion  is  situated  in  the  brain,  the  case  must 
now  be  approached  with  the  view  of  determining  its  exact  seat.  Ordi- 
nary hemiplegia,  when  persistent,  is  caused  most  frequently  by  disease 
of  the  anterior  two-thirds  of  the  posterior  segment  of  the  internal 
capsule  or  of  the  area  of  the  lenticulo-striate  artery.  In  the  most 
usual  form  of  hemiplegia  tlie  arm  is  more  paralyzed  than  the  leg,  but 
in  those  comparatively  rare  cases  in  which  the  leg  is  more  paralyzed 
than  the  arm,  the  motor  paralysis  is  unaccompanied  by  hemianaesthesia, 
and  the  lesion  is  then  situated  in  the  posterior  two-thirds  of  the  pos- 


TOPOGRAPHICAL    DIAGNOSIS.  693 

terior  segment  of  the  internal  capsule  or  in  the  area  of  the  lenticulo- 
optic  artery.  In  some  cases  the  arm  is  more  paralyzed  than  the  leo- 
and  yet  the  hemiplegia  is  accompanied  by  hemianesthesia,  and  the 
lesion  is  then  situated  in  the  optic  thalamus  and  partially  involves  the 
posterior  part  of  the  internal  capsule.  If  the  hemiplegia  is  transient 
the  lesion  is  situated  near  the  motor  tract  without  causing  permanent 
damage  to  its  fibres,  most  commonly  in  the  lenticular  nucleus.  Mono- 
plegia? are  caused  by  lesions  in  the  motor  area  of  the  cortex,  or  in  the 
centrum  semiovale  between  the  motor  centres  and  the  internal  capsule. 
If  the  paralysis  in  such  cases  be  preceded  or  accompanied  by  unilateral 
convulsions,  the  lesion  is  situated  in  or  near  the  cortex.  Monopleo-ie 
caused  by  disease  of  the  motor  cortex  or  of  the  underlying  white  sub- 
stance, are  often  accompanied  by  considerable  diminution  of  the  mus- 
cular sense  and  cutaneous  sensibility  of  the  affected  limb.  The  exact 
situation  of  the  disease  when  the  cortex  or  underlying  white  substance 
is  its  seat,  may  be  determined  by  reference  to  Terrier's  diagrams  and 
Pitre's  vertical  sections  of  the  cerebral  hemispheres.  In  persistent 
motor  aphasia  the  lesion  is  situated  in  the  posterior  part  of  the  third 
frontal  convolution  or  in  the  white  substance  immediately  underlying 
it ;  but  if  recovery  takes  place  in  a  few  weeks  or  months,  it  is  in  or 
near  the  knee  of  the  internal  capsule.  In  sensory  aphasia  the  lesion  is 
situated  in  the  angular  gyrus  or  first  and  second  temporo-sphenoidal 
convolutions,  while  in  mixed  motor  and  sensory  aphasia,  which  is  accom- 
panied by  hemiplegia,  it  is  widely  distributed  over  the  motor  area  of  the 
cortex.  A  transient  aphasia  may  precede  an  attack  of  migraine  head- 
ache, or  follow  a  minor  attack  of  epilepsy.  Hemiansesthesia,  with 
implication  of  the  special  senses,  is  caused  by  disease  of  the  posterior 
part  of  the  internal  capsule.  In  some  of  these  cases  the  visual  affec- 
tion consists  of  an  amblyopia  of  the  eye  on  the  opposite  side  to  the 
lesion,  whilst  in  others  it  consists  of  a  bilateral  hemianopsia.  In  hemi- 
anaesthesia,  with  bilateral  hemianopsia,  the  lesion,  which  is  always 
situated  in  the  optic  thalamus,  reaches  sometimes  so  far  back  as  to 
implicate  the  external  geniculate  body,  but  at  other  times  it  is  situated 
opposite  the  middle  part  of  the  posterior  segment  of  the  internal  cap- 
sule, and  much  too  far  forwards  to  reach  that  body.  A  tumor  in  any 
of  the  basal  ganglia  may  cause  hemianopsia  by  compression  of  the 
underlying  optic  tract.  Homonymous  hemianopsia  may  also  be  caused 
by  a  lesion  in  the  white  substance  or  in  the  cortex  of  the  occipital  lobe. 
Cortical  or  centrum  ovale  hemianopsia  may  be  suspected  rather  than 
tract  hemianopsia  if  the  blind  is  not  separated  from  the  sensitive  area 
of  each  retina  by  a  sharply  defined  straight  line,  if  a  quadrant  only  of 
each   field  is  lost,  or  if  there  is  a  considerable  restriction  of  the  pre- 


694  GENERAL    DIAGNOSIS. 

served  halves  of  the  fields  of  vision,  especially  on  the  side  opposite  the 
lesion.  When  the  lesion  is  situated  in  the  left  hemisphere  the  hemi- 
anopsia is  often  accompanied  by  word-blindness.  In  convulsive  attacks 
which  begin  with  a  visual  aura  consisting  of  colored  vision  or  hallucina- 
tions of  sight,  it  may  be  inferred  that  an  irritative  lesion  is  situated  in 
or  near  the  cortex  of  the  occipital  lobe.  If  the  convulsion  begins  with 
rattling  noises  in  the  ears  or  hallucinations  of  sound,  an  irritative  lesion 
is  situated  in  or  near  the  cortex  of  the  first  or  second  temporo-con- 
volutions. 

It  is  possible  that  a  destructive  lesion  in  this  area  may  give  rise  to 
some  degree  of  deafness  of  the  ear  on  the  opposite  side,  but  this  sign  is 
not  to  be  much  depended  upon.  If  the  lesion,  however,  is  situated  in 
the  left  hemisphere  the  patient  suffers  from  word-deafness,  which  is 
often  accompanied  by  loss  of  smell  in  the  nostril  on  the  side  of  the 
lesion  from  softening  of  the  external  root  of  the  olfiictory  tract.  If  a 
person  who  is  suffering  from  word-deafness  suddenly  becomes  absolutely 
deaf  without  there  being  any  evidence  of  local  disease  of  the  ears,  there 
are  symmetrical  lesions  in  both  temporo-sphenoidal  lobes  on  a  level  with 
the  first  and  second  convolutions. 

Lesions  in  the  remaining  parts  of  the  cortex  of  the  temporo-sphenoidal 
lobe  and  in  the  underlvincr  white  substance  do  not  give  rise  to  definite 
localizing  symptoms,  A  tumor  of  this  lobe  may  by  compressing  the 
optic  tract  give  rise  to  hemianopsia,  and  the  internal  capsule  to  hemi- 
plegia. The  Island  of  Riel  is,  as  we  have  seen,  the  embryonic  area  of 
the  cortex,  and  lesions  of  it  are  often  unaccompanied  by  any  localizing 
symptoms,  but  when  situated  near  the  junction  of  this  lobe  with  the 
operculum  they  give  rise  to  a  motor  aphasia.  IJut  to  return  to  the 
internal  capsule ;  disease  of  the  anterior  segment  does  not  give  rise  to 
any  definite  symptoms.  Charcot  found  softening  of  this  segment  in  a 
case  in  which  there  was  considerable  psychical  disturbance  during  life. 
Disease  of  the  cortex  of  the  prefrontal  area  of  the  brain  with  which  the 
anterior  segment  of  the  internal  capsule  appears  to  be  connected,  is 
also  often  found  in  cases  in  which  there  had  been  considerable  mental 
disorder  during  life.  If  a  patient  with  the  general  symptoms  of  a 
cerebral  disease  lies  in  a  somnolent  condition  without  giving  evidence 
of  localized  sensory  or  motor  disorder,  the  lesion  is  most  probably  situ- 
ated either  in  the  cortex  or  the  white  substance  of  the  prefrontal  lobe. 
In  cases  of  unilateral  convulsions  which  begin  by  spasm  of  the  side  of 
the  face,  if  loss  of  consciousness  precedes  the  spasm,  the  lesion  is  most 
probably  situated  in  the  prefrontal  lobe. 

If  paralysis  of  the  limbs  on  one  side  is  associated  with  paralysis  of 
one  of  the  cranial  nerves  on  the  other,  the  lesion  is  situated  in  or  near 


TOPOGRAPHICAL    DIAGNOSIS.  695 

the  pyramidal  tract  of  the  side  opposite  the  paralyzed  limbs  somewhere 
in  its  course  between  the  internal  capsule  and  the  crossing  in  the  medulla 
oblongata.  When  the  third  nerve  of  one  side  and  the  limbs  on  the 
other  are  simultaneously  paralyzed,  the  lesion  is  in  the  crus  cerebri ; 
when  the  fifth  is  the  cranial  nerve  affected,  the  lesion  is  situated  about 
the  middle  of  the  pons ;  when  the  sixth  or  seventh,  the  seat  is  about 
the  lower  or  posterior  end  of  the  pons  ;  and  Avhen  the  twelfth,  it  is 
localized  in  the  medulla,  but  the  last  occurs  only  very  rarely.  In  apo- 
plectic lesions  of  the  upper  part  of  the  pons  the  pupils  are  often  strongly 
contracted  from  irritation  of  the  nuclei  of  the  third  nerve.  In  partial 
anaesthesia  of  one  side  of  the  face  and  anaesthesia  of  the  trunk  and 
limbs  on  the  opposite  side,  the  lesion  is  situated  in  the  restiform  body  in 
or  near  the  ascending  root  of  the  fifth  nerve.  Unilateral  lesions  of  the 
pons  implicate  the  transverse  fibres  coming  from  the  middle  peduncle 
of  the  cerebellum,  and  consequently  give  rise  to  a  tendency  to  fall  to 
the  side  of  the  lesion. 

Disease  of  the  basal  ganglia  do  not  give  rise  to  very  definite  symp- 
toms, except  when  they  are  sufficiently  large  to  compress  or  rupture  the 
fibres  of  the  internal  capsule.  If  a  patient  has  sufiered  from  a  slight 
apoplectic  attack  with  right  hemiplegia  and  aphasia,  from  which  recovery 
takes  place  in  a  few  weeks  leaving  only  a  slight  exaggeration  of  the 
tendon  reflexes  at  the  wrist,  the  lesion  is  most  probably  a  hemorrhage 
limited  to  the  left  lenticular  nucleus.  If  the  same  patient  has,  some 
time  afterwards,  a  second  apoplectic  attack  with  left-sided  hemiplegia 
and  aphasia,  from  which  recovery  also  takes  place  in  the  course  of  a  few 
weeks,  leaving,  in  addition  to  a  slight  exaggeration  of  the  tendon-reflexes 
at  the  left-wrist,  bulbar  symptoms  like  those  of  progressive  labio-glosso- 
pharyngeal  paralysis,  both  lenticular  nuclei  will  most  probably  be  found 
to  have  been  destroyed  by  hemorrhage.  Lesions  strictly  limited  to  the 
caudate  nucleus  or  to  the  inner  half  of  the  optic  thalamus  cause  no 
localizing  symptoms.  If,  however,  a  person  has  a  slight  apoplectic 
attack  which  is  at  first  attended  with  little  or  no  loss  of  consciousness, 
and  becomes  after  a  few  minutes  or  hours  suddenly  profoundly  comatose 
with  complete  resolution  of  all  the  limbs,  or  paralysis  of  the  limbs  on 
one  side  and  spasmodic  contraction  of  those  on  the  other,  dilated  and 
fixed  pupils,  and  a  great  initial  lowering  followed  by  a  rapid  rise  of  tem- 
perature, a  hemorrhage  of  the  caudate  nucleus  or  of  the  inner  part  of 
the  optic  thalamus  has  ruptured  into  the  general  ventricular  cavity. 

When  an  apoplectic  attack  causes  hemiplegia  with  hemianaesthesia, 
which  is  followed  by  post-hemiplegic  chorea  or  athetosis,  the  lesion  is 
situated  in  the  area  of  the  posterior  external  artery  of  the  optic  thalamus, 
but  it  is  not  known  whether  the  mobile  spasms  are  caused  by  the  damage 


696  GENERAL    DIAGNOSIS. 

done  to  the  ganglion  itself  or  by  partial  injury  of  the  internal  capsule. 
Bilateral  athetosis  and  the  choreic  movements  which  attend  some  of  the 
spasmodic  paralyses  of  infancy  are  caused  by  a  parencephalus  or  uni- 
lateral atrophy  of  the  motor  area  of  the  cortex  of  the  brain.  If  a 
severe  apoplectic  attack,  followed  by  a  prolonged  period  of  partial  un- 
consciousness and  death  after  a  few  weeks,  is  attended  by  hemiplegia 
and  hemiangesthesia,  rotation  of  one  eyeball  downwards  and  outwards 
and  of  the  other  upwards  and  outwards,  dilating  pupils  on  exposure  to 
light,  and  paroxysms  of  Cheyne-Stokes  breathing,  the  lesion  Avill  be 
found  to  have  been  a  hemorrhage  which  has  completely  destroyed  the 
whole  of  the  pulvinar  of  the  optic  thalamus  with  the  posterior  part  of 
the  internal  capsule,  and  to  have  made  its  way  inwards  so  as  to  be  only 
separated  from  the  cavity  of  the  third  ventricle  by  a  thin  layer  of  tissue, 
and  backwards  so  as  to  have  undermined  and  partially  destroyed  the 
anterior  tubercle  of  the  corpora  quadrigemina.  Lesions  which  are 
more  or  less  limited  to  the  corpora  quadrigemina  do  not  probably  give 
rise  to  distinctive  symptoms,  and  the  same  remark  applies  to  lesions  of 
the  corpus  callosum,  although  cases  of  tumor  in  this  situation  have  been 
recorded  by  Erb  and  Bristow. 

Loss  of  one  or  more  of  the  functions  of  the  cranial  nerves  suggests 
the  possibility  of  an  intracranial  growth  at  the  base  of  the  brain,  or  a 
basal  meningitis.  Complete  loss  of  smell  with  the  presence  of  double 
optic  neuritis,  or  other  symptoms  of  a  chronic  intracranial  disease,  indi- 
cates a  growth  in  the  anterior  fossa  of  the  skull.  Complete  loss  of 
sight  of  one  eye,  with  atrophy  of  the  optic  disk  and  paralysis  of  the 
oculo-motor  nerves  and  of  the  ophthalmic  division  of  the  fifth,  indicates 
most  probably  a  chronic  meningitis  with  much  thickening  around  the 
optic  foramen  and  temporo-sphenoidal  fissure.  If,  in  addition  to  these 
symptoms,  there  is  temporal  hemianopsia  of  the  other  eye,  the  lesion  is 
a  tumor  situated  over  the  cavernous  sinus  and  coming  as  far  forwards 
as  the  optic  foramen.  The  presence  of  double  temporal  liemianopsia 
shows  pressure  on  the  centre  of  the  optic  commissure  either  by  tumor  of 
the  sella  Turcica  or  rarely  by  distention  of  the  third  ventricle  by  fluid. 
As  the  lesion  increases  in  size  complete  blindness  may  result,  but  most 
frequently  it  grows  to  one  side  and  gives  rise  to  blindness  of  one  eye, 
with  temporal  hemianopsia  of  the  other. 

When  hyper?esthesia  or  anaesthesia  in  the  area  of  distribution  of  the 
fifth  nerve  is  accompanied  by  neuroparalytic  ophthalmia,  with  or  without 
masticatory  paralysis,  the  lesion  is  likely  to  be  situated  in  the  middle 
fossa  of  the  skull,  and  when  both  third  nerves  are  paralyzed  in  associa- 
tion with  some  degree  of  single  or  double  hemiplegia,  and  the  general 
symptoms  which  indicate  an  intracranial  growth  or  abscess,  the  lesion 


TOPOGRAPHICAL    DIAGNOSIS. 


697 


is  situated  in  the  interpeduncular  space.  When  the  fifth  and  sixth, 
the  seventh  and  eighth,  or  the  eleventh  and  twelfth  nerves  are  simul- 
taneously paralj^zed,  the  lesion  is  likely  to  be  in  the  posterior  fossa  of 
the  skull  rather  than  in  the  substance  of  the  pons  and  medulla  ob- 
longata. When  a  tumor  is  situated  near  the  cortex  of  the  brain  the 
skull  is  often  tender  to  percussion  at  the  the  point  at  which  the  growth 
comes  nearest  to  the  surface. 


View  of  the  Posterior  Surface  of  the  Mepulla  (after  Erb), 
the  roof  of  the  fourth  ventricle  being  removed  to  show  the  rhomboid  sinus  clearly.  The  left  half  of  the 
figure  represents:  On,  funiculus  cuneatus,  and  g.  funiculus  gracilis;  0,  obex;  sp,  nucleus  of  the  spinal 
accessory ;  p,  nucleus  of  pneumogastric,  p  +  sp,  ala  cinera  ;  R,  restiform  body  ;  XII',  nucleus  of  the 
hypoglossal;  t,  funiculus  teres;  a,  nucleus  of  the  acousticus  ;  m,,  strife  meduUares  ;  1,  2,  and  3,  middle, 
superior,  and  inferior  cerebellar  peduncles  respectively  ;  /,  fovea  anterior  ;  4,  eminentia  teres  (genu  nervi 
facialis)  ;  5,  locus  coeruleus.  The  right  half  of  the  figure  represents  the  nerve  nuclei  diagrammatically  ; 
V,  motor  trigeminal  nucleus ;  V,  median,  and  V",  inferior  sensory  trigeminal  nuclei ;  VI,  nucleus  of 
abducens  ;  VII,  facial  nucleus ;  VIII,  posterior  median  acoustic  nucleus ;  VIII'  anterior  median, 
VIII"  posterior  lateral,  VIII'"  anterior  lateral  acoustic  nuclei ;  IX,  glosso-pharyngeal  nucleus  ;  X,  XI, 
and  XII,  nuclei  of  vagus,  spinal  accessory,  and  hypoglossal  nerves  respectively.  The  Roman  numerals 
at  the  side  of  the  figure,  from  V  to  XII,  represent  the  corresponding  nerve  roots 

When  the  lesion  is  situated  in  the  spinal  cord  below  the  crossing  of 
the  pyramidal  tracts,  it  gives  rise  to  a  spasmodic  paralysis  of  all  muscles 
innervated  from  below  the  level  of  the  disease,  as  well  as  to  more  or 
less  anaesthesia  of  the  inferior  part  of  the  body.  The  muscles  supplied 
from  the  level  of  the  lesion  suffer  from  atrophic  paralysis,  the  reflexes 


698 


GENERAL    DIAGNOSIS, 


of  the  affected  segment  of  the  cord  are  abolished,  and  a  line  of  hyperaes- 
thesia  passing  round  the  body  generally  sepai'ates  the  anaesthetic  and 
sensitive  areas. 

In  the  various  forms  of  atrophic  paralysis  the  situation  of  the  lesion 
must  be  inferred  from  the  grouping  of  the  affected  muscles.  In  oph- 
thalmoplegia externa  the  lesion  is  situated  in  the  nuclei  of  the  third 

Fig   184. 


Transparent  Lateral  View  of  the  Mediila  (alter  Erb), 
showing  the  relative  positions  of  tlie  most  important  nuclei  ;  right  half  of  the  medulla,  seen  from  the 
surface  of  section  ;  the  parts  that  lie  closer  to  this  surface  are  deeiH'r  shaded.  Diagrammatic.  Vy,  pyra- 
midal tract;  Py,  Kr,  decussation  of  pyramids;  0,  olivary  body;  0»,  superior  olivary  body;  V,  motor, 
V,  middle  sen.sory  ;  V",  inferior  sensory  nucleus  of  trigeminus;  VI,  nucleus  of  abducens;  c.f,  genu 
facialis  nervi ;  VII,  nucleus  facialis  ;  VIII,  posterior  median  acoustic  nucleus ;  IX,  glosso-pharyngeal 
nucleus;  X,  nucleus  of  vagus;  XI,  nucleus  of  the  acrcssorius ;  XII,  hypoglossal  nucleus;  Kz,  nucleus 
of  the  funiculus  gracilis;  Rv,  trigeminus  root;  RVI,  roof  of  the  abducens  ;  KVII,  root  of  facialis 

and  sixth  nerves;  in  progressive  labio-glosso-laryngeal  paralysis  and 
the  acute  form  of  the  affection  caused  by  occlusion  of  a  branch  of  the 
basilar  artery,  the  lesion  is  situated  in  the  inferior  part  of  the  floor  of 
the  fourth  ventricle  (Figs.  183  and  184);  and  in  the  usual  forms  of 
acute  atrophic  spinal  paralysis  of  infants  and  adults  the  lesion  is  situated 
in  the  anterior  gray  horns  of  the  spinal  cord,  the  exact  level  of  the 


PATHOLOGICAL    DIAGNOSIS.  699 

lesion  in  the  longitudinal  extent  of  the  cord  being  indicated  by  the 
particular  muscles  attacked  as  well  as  by  the  reflexes  which  are  found 
abolished. 

When  an  atrophic  paralysis  is  restricted  to  the  muscles  supplied  by 
a  particular  nerve,  and  Avhen  there  is  at  the  same  time  more  or  less 
anaesthesia  in  the  area  of  distribution  of  the  sensory  branches,  the 
lesion  is  situated  in  the  peripheral  course  of  the  nerve.  In  atrophic 
paralysis  from  disease  of  nerves  the  muscles  are  affected  according  to 
the  distribution  of  the  branches  of  the  diseased  nerve,  but  in  spinal 
atrophic  paralysis  they  are  affected  in  groups  according  as  they  are 
associated  in  their  functions.  If  the  motor  disorder  consists  of  an 
incoordination  and  not  of  a  spasm  or  paralysis,  the  disease  is  likely  to  be 
either  tabes  dorsalis,  Meniere's  disease,  sclerosis  in  patches,  or  a  cere- 
bellar lesion.  In  tabes  the  patellar  tendon-reflexes  are  absent,  and  the 
gait  is  ataxic;  in  Meniere's  disease  the  patient  is  deaf  and  suft'ers  from 
whistling  noises  in  the  ears ;  in  multiple  sclerosis  the  patellar  tendon- 
reactions  are  generally  exaggerated,  and  the  patient  manifests  the 
tremor,  scanning  speech,  and  other  characteristic  phenomena,  while  in 
cerebellar  disease  the  patellar  tendon-reactions  are  generally  exaggerated, 
and  the  salt  is  a  reel  and  not  a  true  ataxia. 


3.  PATHOLOGICAL  DIAGNOSIS. 

The  aim  of  pathological  diagnosis  is  to  determine  the  nature  of  the 
lesion  no  matter  where  it  may  be  situated.  It  may  be  laid  down  as  a 
general  rule,  but  one  requiring  numerous  qualifications  in  practice,  that 
the  diseases  which  develop  the  symptoms  of  depression  in  the  course  of 
a  few  minutes  or  a  few  hours,  and  without  being  set  up  by  traumatic  or 
toxic  causes,  are  of  vascular  origin ;  that  the  diseases  which  take  from 
a  few  days  to  a  few  weeks  for  the  full  development  of  the  symptoms, 
and  in  which  the  symptoms  of  depression  are  preceded  by  those  of 
irritation,  are  of  inflammatory  origin;  and  that  the  diseases  which  take 
from  two  to  six  months  for  the  full  development  of  their  symptoms, 
and  in  which  the  primary  symptoms  of  irritation  are  either  absent  or 
obscured  by  the  more  prominent  symptoms  of  depression,  are  of  degen- 
erative origin,  or  are  due  to  a  slow  and  gradual  compression  of  nervous 
tissue  by  the  growth  of  a  new  formation. 

(1)  Vascular  Lesions. — The  vascular  lesions  Avhich  are  the  most 
frequent  causes  of  disease  of  the  nervous  system  are  rupture  with  hem- 
orrhage, embolism,  and  thrombosis.  If  a  patient  suddenly  becomes 
profoundly  comatose  without  premonitory  symptoms,  and  with  or  with- 


700  GENERAL    DIAGNOSIS. 

out  evidence  of  the  presence  of  hemiplegia,  the  lesion  is  more  likely  to 
be  a  hemorrhage  rather  than  embolism  or  thrombosis.  If  the  coma 
passes  off  in  a  few  hours  or  days  Avithout  leaving  a  trace  of  hemiplegia 
or  other  grave  symptoms,  the  lesion  has  probably  been  a  cerebral  conges- 
tion, but  if  the  coma  has  been  somewhat  prolonged,  and  if  hemiplegia 
persists,  the  lesion  has  been  a  hemorrhage.  Hemorrhage  is  to  be  sus- 
pected rather  than  embolism  if  an  apoplectic  attack  occurs  during  the 
degenerative  period  of  life  or  after  forty-five  years  of  age ;  if  the  arteries 
at  the  wrist  and  temples  are  hard  and  knotty;  if  the  left  ventricle  of 
the  heart  is  hypertrophied ;  if  the  second  sound  of  the  heart  is  much 
accentuated  at  the  base;  if  the  urine  is  abundant  and  of  low  specific 
gravity,  and  if  it  contains  a  small  quantity  of  albumen ;  if  the  arterial 
tension  is  high ;  and  if  a  well-marked  arcus  senilis  and  other  signs  of 
degeneration  of  tissue  are  present.  Ingravescent  apoplexy  is  almost 
always  caused  by  hemorrhage,  and  when  this  form  of  hemorrhage 
occurs  in  comparatively  young  people  it  may  be  suspected  that  an 
aneurism  has  burst.  If  an  apoplectiform  attack,  with  or  without  hemi- 
plegia, occur  in  a  young  or  middle-aged  person  who  is  suffering  from 
valvular  disease  of  the  heart,  the  lesion  is  likely  to  be  eml)olism.  This 
supposition  is  strengthened  if  the  onset  of  the  disease  was  not  attended 
by  a  profound  loss  of  consciousness,  and  if  a  more  or  less  persistent 
aphasia  is  established.  Embolism  is,  indeed,  more  probable  than  hem- 
orrhage if  the  attack  has  supervened  during  the  course  of  acute  rheuma- 
tism, chorea,  or  scarlet  fever,  even  when  no  signs  of  valvular  disease 
can  be  discovered.  Valvular  disease  may  give  rise  to  an  aneurism  of  a 
cerebral  vessel  and  to  subsequent  rupture,  and  conseijuently  the  signs  of 
cardiac  disease  are  only  of  value  in  determining  the  question  of  em- 
bolism or  hemorrhage  when  taken  in  conjunction  with  other  symptoms. 

Thrombosis  of  the  arteries  of  the  brain  occurs  in  old  aije  from  atheroma 
and  in  middle  age  from  syphilitic  endarteritis. 

Occlusion  of  a  cerebral  artery  by  thrombosis  gives  rise  to  an  apoplectic 
attack  like  that  caused  by  an  embolus,  but  in  the  former  the  attack  is 
preceded  by  premonitory  symptoms  which  are  wanting  in  the  latter,  and 
the  attack  itself  is  often  more  gradual  in  its  development  in  thrombosis 
than  either  in  embolus  or  hemorrhage.  The  premonitory  symptoms 
of  thrombosis  consist  of  headache,  dizziness,  loss  of  memory,  and 
general  confusion,  together  with  numbness  and  formication  of  one  of  the 
limbs  or  of  one-half  the  body.  Syphilitic  thrombosis  is  often  preceded 
by  severe  headache  with  nocturnal  exacerbations,  while  other  evidences  of 
syphilis  may  be  obtained. 

If  an  apoplectic  attack  supervenes  in  the  puerperal  state,  or  in  the 
course  of  exhausting  diseases  like  phthisis  and  cancer,  and  in  children 


PATHOLOGICAL    DIAGNOSIS.  701 

after  severe  diarrhoea,  the  cause  is  most  likely  a  thrombosis  of  one  of 
the  cerebral  veins  or  sinuses.  It  is  also  probable  that  the  condition 
known  as  asphyxia  neonatorum,  and  which  is  followed  by  a  spasmodic 
paralysis  with  idiocy,  is  caused  by  thrombosis  of  one  of  the  cerebral 
veins  occasioned  by  injury  to  the  head  during  delivery. 

Hemorrhage  of  the  spinal  cord  occurs  in  comparatively  young  subjects. 
It  is  liable  to  be  mistaken  for  acute  spinal  atrophic  paralysis,  from  which 
it  may  be  distinguished  by  the  fact  that  the  atrophic  paralysis  caused  by 
the  local  lesion  is  in  hemorrhage  accompanied  by  sensory  disorders  and 
by  spasmodic  paralysis  caused  by  implication  of  the  posterior  horns  and 
the  sensory  and  motor  conducting  paths. 

(2)  Inflammatory  Lesions. — The  inflammatory  nature  of  the  lesion 
must  be  determined  by  the  mode  of  onset  being  more  gradual  than  in 
vascular  lesions ;  the  symptoms  of  depression  being  preceded  by.  those 
of  irritation,  and  the  presence  during  the  development  of  the  disease  of 
elevation  of  temperature  and  other  febrile  sym.ptoms.  When  once  it  is 
concluded  that  the  lesion  is  inflammatory  the  further  classification  of 
the  disease  must  be  determined  from  the  grouping  of  the  symptoms  and 
the  localization  of  the  lesion. 

(3)  Degenerative  Lesions. — It  is  difiicult  to  draAv  any  definite  line  of 
demarcation  between  the  secondary  degenerations,  which  result  from 
chronic  inflammation,  and  those  diseases  which  are  of  degenerative  orio-in 
from  the  commencement.  The  development  of  the  disease  may  be 
chronic  and  progressive  in  both,  and  the  chief  reliance  in  diagnosis 
must  be  placed  upon  the  presence  of  symptoms  of  irritation  and  slight 
elevation  of  temperature  in  the  former  and  their  absence  in  the  latter. 

Multiple  cerebro-spinal  sclerosis  is  a  chronic  degenerative  disease, 
probably  of  inflammatory  origin,  which,  from  the  variability  of  its  symp- 
toms, is  liable  to  be  mistaken  for  various  other  diseases.  It  would  be 
difficult  to  believe  that  paralysis  agitans  and  multiple  cerebro-spinal 
sclerosis  were  confounded  with  one  another,  were  it  not  a  matter  of 
history  that  the  two  diseases  were  only  separated  from  one  another 
clinically  for  the  first  time  by  Charcot  only  a  few  years  ago.  Multiple 
sclerosis  is  a  disease  of  youth  and  middle  age,  and  paralysis  agitans 
most  commonly  of  advanced  age.  The  tremor  of  paralysis  agitans 
consists  of  fine  rapid  oscillations,  which  persist  during  repose ;  it  may  be 
temporarily  arrested  by  voluntary  effort,  and  seldom  implicates  the 
muscles  of  the  head ;  while  the  tremor  of  multiple  sclerosis  has  a  some- 
what extensive  sweep,  ceases  during  repose,  is  excited  or  aggravated  by 
voluntary  movements,  and  almost  always  implicates  the  muscles  of  the 
head.  In  paralysis  agitans  decided  loss  of  motor  power  is  not  developed 
until  long  after  the   appearance   of  tremor,  but   in  multiple  sclerosis 


702  GENERAL    DIAGNOSIS. 

paralysis  precedes  or  soon  follows  the  tremor.  The  nystagmus,  scanninfr 
speech,  and  other  cerebral  symptoms  of  multiple  sclerosis  are  wanting 
in  paralysis  agitans. 

Multiple  sclerosis,  especially  in  its  early  stages,  may  be  mistaken  for 
some  one  or  other  of  the  system  diseases  of  the  spinal  cord,  such  as 
locomotor  ataxia,  primary  lateral  sclerosis,  amyotrophic  lateral  sclerosis, 
or  progressive  labio-glosso-laryngeal  paralysis,  and  it  is  not  always 
possible  to  be  sure  of  the  diagnosis  until  symptoms  like  nystagmus, 
scanning  speech,  and  tremor  appear  in  the  course  of  the  disease,  which 
are  more  or  less  characteristic  of  multiple  sclerosis,  and  never  form  jiart 
of  the  system  diseases.  The  hereditary  form  of  locomotor  ataxia  de- 
scribed by  Friedreich  is  probably  more  allied  to  nmltiple  sclerosis  than 
to  the  tabes  dorsalis  of  adults.  Mercurial  tremor  is  sometimes  so  like 
a  moderately  advanced  case  of  multiple  sclerosis  that  the  former  can 
only  be  recognized  from  the  latter  by  the  history  of  exposure  to  its 
cause.  Hysterical  tremor  persists  during  repose,  provided  the  patient  is 
conscious  of  being  observed  ;  it  may  disappear  for  a  long  time  and  then 
recur,  and  general  hysterical  symptoms  are  usually  present.  The  dis- 
orderly movements  of  chorea  differ  considerably  from  the  tremor  of 
multiple  sclerosis,  but  the  diagnosis  is  not  always  easy  when,  as  may 
occasionally  happen,  choreiform  movements  complicate  those  proper  to 
multiple  sclerosis. 

The  early  stage  of  general  paralysis  of  the  insane  may  very  readily 
be  mistaken  for  the  early  stage  of  multiple  sclerosis.  The  hesitating 
and  indistinct  speech  of  general  paralysis  is  very  like  the  scanning 
speech  of  multiple  sclerosis,  and  the  tremors  of  the  tongue  and  angle  of 
the  mouth  and  of  the  hands  in  the  former,  may  be  mistaken  for  the 
tremor  which  is  so  characteristic  of  the  latter  disease ;  wiiile  the  patellar 
tendon- react  ions  may  be  either  exaggerated  or  absent  in  both  diseases. 
The  age  at  which  patients  are  attacked  affords  some  help  in  diagnosis, 
multiple  sclerosis  being  most  common  in  the  first  three,  and  general 
paralysis  in  the  fourth  decade  of  life.  Inequality  of  the  pupils  and  loss 
of  the  light-retlex  are  common  in  general  paralysis,  and  ])robably  never 
occur,  especially  together,  in  multiple  sclerosis.  When  the  characteristic 
expansive  delirium  with  grand  ideas,  of  general  paralysis  is  well  marked, 
the  diagnosis  is  easy,  and  even  in  the  man}'  cases  in  which  it  is  absent 
the  patient  has  a  peculiar  air  of  contentment  and  self-satisfaction  which 
is  wanting  in  multiple  sclerosis.  The  diagnosis  becomes  more  easy  with 
the  advance  of  these  diseases.  In  general  paralysis  the  ])atient  mani- 
fests distinct  signs  of  loss  of  memory  and  decided  mental  failure,  while 
in  multiple  sclerosis  the  mental  condition  is  generally  one  simply  of 
emotional  excitability,  and  only  rarely  of  pronounced  mental  failure. 


PATHOLOGICAL    DIAGNOSIS.  703 

and  in  these  occasional  eases  other  characteristic  symptoms,  like  nystag- 
mus and  a  widely  diffused  tremor,  are  present  to  make  the  nature  of  the 
disease  sufficiently  clear. 

(4)  Neiv  Formations. — When  a  patient  suffers  from  a  severe  and 
persistent  headache,  dizziness,  and  vomiting,  the  existence  of  an  intra- 
cranial growth  ought  to  he  suspected,  and  the  presence  of  double  optic 
neuritis  places  the  diagnosis  almost  beyond  question.  The  localizing 
symptoms  met  with  in  cases  of  cerebral  tumor  are  the  same  generally 
as  those  caused  by  hemorrhage  and  focal  diseases,  but  these  symptoms 
creep  on  gradually  and  progressively  in  tumor,  and  not  suddenly  as  in 
the  vascular  diseases.  Paralysis  and  other  localizing  symptoms  may, 
however,  occur  in  the  course  of  a  tumor  from  a  complicating  hemor- 
rhage, or  oedema  of  the  brain,  or  occlusion  of  a  vessel  from  compression. 

When  once  it  is  concluded  that  a  foreign  body  is  encroaching  upon 
the  cranial  cavity,  the  next  question  to  be  determined  is  the  nature  of 
this  growth.  If  the  symptoms  of  an  intracranial  growth  are  found  in 
a  young  person  of  tubercular  diathesis,  and  especially  if  the  presence 
of  cavities  in  the  chest,  of  enlargement  of  glands,  or  of  a  chronic  dis- 
charge from  the  ear  indicate  tubercular  disease  of  other  organs,  then 
the  cerebral  disease  is  likely  to  be  a  tubercular  tumor.  This  supposition 
is  strengthened  if  the  symptoms  indicate  that  the  tumor  is  situated  in 
the  pons,  cerebellum,  or  cortex  of  the  brain;  if  the  progress  of  the 
case  is  somewhat  rapid  ;  and  if  there  are  signs  of  the  presence  of 
multiple  lesions. 

If  the  symptoms  of  an  intracranial  growth,  indicating  the  same 
localization  as  that  of  the  tubercular  tumor,  occur  in  an  otherwise  healthy 
young  person  who  is  free  from  syphilitic  taint,  the  tumor  is  likely  to  be 
a  glioma.  This  supposition  Avill  be  strengthened  if  the  development  of 
the  symptoms  had  been  preceded  by  an  injury  to  the  skull,  and  if  tlie 
progress  of  the  disease  is  comparatively  slow.  If  the  chief  symptom 
of  an  intracranial  growth  is  caused  by  compression  of  the  nerves  at  the 
base  of  the  skull,  the  tumor  is  likely  to  be  a  sarcoma.  This  supposition 
is  strengthened  if  the  progress  of  the  disease  is  slow  and  progressive, 
and  the  diagnosis  is  rendered  almost  certain  if  a  sarcomatous  growth 
is  discovered  in  any  other  organ.  If  a  patient  about  middle  age 
suffering  from  the  symptoms  of  an  intracranial  growth,  has  a  cachectic 
appearance,  if  the  disease  makes  rapid  progress,  and,  above  all,  if  there 
is  evidence  that  cancer  is  deposited  in  other  organs,  then  the  growth  is 
likely  to  be  cancer. 

If  the  symptoms  of  an  intracranial  growth  are  attended  by  marked 
psychical  disturbances,  and  convulsions,  which  are  at  first  unilateral 
and  occasionally  become  general  and  frequently  repeated  near  the  fatal 


70-i  GENERAL    DIAGNOSIS. 

termination,  and  if  these  symptoms  occur  in  a  butcher  or  pork-dealer, 
or  in  one  who  has  suffered  from  tapeworm,  then  the  tumor  is  likely  to 
be  cysticercus  cellulosce.  The  diagnosis  of  the  presence  of  echinocoeci 
in  the  brain  must  be  made  from  the  general  symptoms  of  intracranial 
tumor  appearing  and  disappearing  alternately,  a'dema  of  the  eyelids, 
an  opening  in  the  cranial  bones  through  which  a  fluctuating  tumor  pro- 
jects, or  exploratory  puncture. 

Abscess  of  the  brain  occurs  as  the  direct  consequence  of  an  injury, 
such  as  fracture  of  the  skull  and  contusion  of  the  brain,  or  is  associated 
with  some  other  disease,  such  as  caries  of  the  petrous  portion  of  the 
temporal  bone,  and  oz?ena,  and  the  presence  of  suppuration  is  often 
indicated  by  rigors  and  fever.  A  cerebral  abscess  may  remain  more  or 
less  latent  for  a  long  period,  and  then  the  patient  is  suddenly  attacked 
Avith  symptoms  like  those  of  meningitis  or  becomes  rapidly  comatose. 
If  a  person  beyond  middle  life  is  the  subject  of  heart  disease,  extensive 
arterial  degeneration,  or  syphilis,  and  is  at  the  same  time  suffering 
from  the  symptoms  of  a  tumor  situated  at  the  base  of  the  brain,  an 
aneurism  of  one  of  the  arteries  of  the  brain  may  be  suspected,  and  this 
suspicion  will  be  confirmed  provided  a  murmur  is  audible  on  auscultation 
of  the  skull.  It  is  probable  that  aneurisms  cause  more  pronounced 
symptoms  of  irritation  than  otlier  growths,  consisting  of  intense  cepha- 
lalgia, paroxysms  of  severe  and  intractable  trigeminal  neuralgia,  and 
attacks  of  mania  and  other  grave  psychical  disorders.  If  a  patient  who 
has  been  suffering  from  the  symptoms  of  a  basal  tumor  die  suddenly 
from  an  attack  of  ingravescent  apoplexy,  it  may  be  conjectured  that  the 
tumor  has  been  an  aneurism.  If  a  patient  suffering  from  a  tumor  in 
the  anterior  fossa  of  the  skull  die  suddenly  after  a  copious  hemorrhage 
from  the  nose,  it  may  be  assumed  that  an  aneurism  of  the  anterior  cerebral 
artery  has  perforated  the  cribriform  j)late  of  the  ethmoid  bone.  If 
pulsation  and  a  murmur  on  auscultation  be  observed  in  the  orbit  in)ine- 
diately  after  an  injury  to  the  skull,  it  is  probable  that  a  communication 
has  been  established  between  the  internal  carotid  and  cavernous  sinus. 
The  localizing  symptoms  of  intracranial  aneurisms  are  the  following: 
aneurisms  of  the  anterior  cerebral  and  anterior  communicating  arteries 
cause  loss  of  smell  and  probably  also  unilateral  blindness ;  aneurism  of 
the  internal  carotid  causes  intractable  facial  neuralgia,  paralysis  of  the 
motor  nerves  of  the  eyeball,  blindness  of  one  eye  and  temporal  hemi- 
anopsia of  the  other.  It  may  also  cause  complete  facial  paralysis,  Avith 
distortion  of  the  uvula  and  complete  deafness  on  the  side  of  the  lesion. 
Aneurism  of  the  posterior  communicating  artery  causes  paralysis  of 
the  third  nerve  with  or  without  hemianopsia  ;  aneurism  of  the  posterior 
cerebral  artery  or  of  the  superior  cerebellar  artery  causes  paralysis  of 


PATHOLOGICAL    DIAGNOSIS.  705 

the  third  nerve  of  the  sanae  side  and  hemiplegia  of  the  opposite  side. 
Aneurism  of  the  upper  part  of  the  basilar  causes  paralysis  of  the  fifth 
and  sixth  nerves  with  bilateral  weakness  of  the  limbs,  and  aneurism  of 
the  lower  part  of  the  basilar  or  of  the  vertebral  artery  causes  symptoms 
of  bulbar  paralysis  with  unilateral  or  bilateral  weakness  of  the  limbs. 
Occipital  pain  is  also  a  symptom  of  aneurism  of  the  basilar  artery. 

Tumors  of  the  vertebral  canal  and  spinal  cord,  and  of  the  peripheral 
nerves,  have  already  been  sufficiently  considered,  and  we  shall  now  make 
a  few  general  remarks  on  syphilis  of  the  nervous  system,  a  subject  which 
we  have  purposely  reserved  to  the  last.  There  is  scarcely  any  orcranic 
disease  of  the  nervous  system  but  may  be  simulated  by  syphilitic  lesions. 

Syphilis  may  cause  periostitis,  osteitis,  exostoses,  and  caries  of  bones, 
which  will  first  irritate  and  subsequently  destroy  neighboring  nervous 
structures.  When  the  vertebrae  or  bones  of  the  skull  are  afi'ected,  the 
spinal  or  cerebral  dura  mater  becomes  thickened,  and  thus  a  chronic 
pachymeningitis  is  constituted  which  damages  the  roots  of  the  nerves  as 
they  pass  outwards  to  the  intervertebral  foramina,  or  along  the  base  of 
the  skull.  Gummata  may  form  in  the  dura  mater,  where  they  become 
encapsulated  and  injure  the  spinal  cord  or  brain  only  by  pressure;  or 
in  the  subarachnoid  space,  and  then  the  nerves,  bloodvessels,  and  the 
nervous  structures  themselves  are  involved  in  the  growth.  Gummata 
may  also  grow  in  the  sheaths  of  the  peripheral  nerves,  and  the  cranial 
nerves  are  often  implicated  at  their  points  of  origin  and  before  they 
have  become  covered  by  a  prolongation  of  the  dura  mater.  In  other 
cases  gummatous  tissue  forms  a  diffused  infiltration  in  the  substance  of 
the  nervous  tissues,  instead  of  forming  a  circumscribed  growth.  In 
many  cases  this  infiltration  undergoes  a  partial  organization,  and  it 
then  gives  rise  to  a  chronic  sclerosis  which  may  alFect  one  of  the  phy- 
siological tracts  of  the  spinal  cord,  or  a  localized  portion  of  the  brain, 
or  it  is  disseminated  in  patches  throughout  the  brain  and  spinal  cord. 
When  the  syphilitic  infiltration  occurs  in  the  membranes  it  renders  the 
tissues,  on  being  partially  organized,  dense,  inelastic,  and  opaque,  and 
causes  adhesions  between  the  dura  and  pia  mater,  and  between  the 
latter  membrane  and  the  brain.  In  such  cases  the  neighboring  nervous 
tissues  are  imperfectly  nourished  owing  to  the  retraction  of  the  lumen 
of  the  bloodvessels.  The  arteries  of  the  body,  as  a  whole,  arc  liable  to 
undergo  chronic  changes  in  syphilis,  caused  by  an  endarteritis,  which 
may  ultimately  lead  to  the  formation  of  aneurisms  in  various  parts  and 
occlusion  of  arteries  by  thrombosis,  or  even  by  embolism,  or  to  rupture 
and  hemorrhage.  Syphilitic  diseases  of  the  bones  and  gummata  may 
act  like  foreign  bodies  and  set  up  a  more  or  less  acute  inflammation 
of  neisrhborino;  nerve  structures,  and  thus  extensive  inflammatory  affec- 

45 


706  GENERAL    DIAGNOSIS. 

tions  which  are  not  at  all  syphilitic  in  their  own  nature,  may  be  origi- 
nated by  this  poison,  and  when  once  a  sclerosis  of  nervous  tissue  is  set 
up  by  a  syphilitic  lesion,  it  is  probable  that  the  process  will  pursue  a 
progressive  course  independently  of  the  syphilitic  poison.  Syphilis 
appears  also  to  favor  the  appearance  of  acute  diseases  of  the  nervous 
system  without  the  presence  of  any  lesion  which  is  distinctively  syphilitic. 
Acute  ascending  paralysis,  for  example,  has  been  observed  with  prepon- 
derating frequency  in  syphilitic  subjects,  but  an  examination  of  the 
nervous  tissues  has  not  led  to  the  discovery  of  any  characteristic  syphi- 
litic lesion. 

In  the  peripheral  nerves  syphilis  gives  rise  occasionally  to  acute, 
more  frequently  to  chronic  neuritis,  and  to  compression  of  both  spinal 
and  cranial  nerves  by  the  formation  of  gummata.  In  the  spinal  cord 
it  tends  to  produce  acute  ascending  spinal  paralysis  and  probably  acute 
spinal  meningitis  and  acute  myelitis,  and  it  likewise  causes,  with  varia- 
ble frequency,  chronic  spinal  meningitis,  chronic  myelitis,  lateral  spinal 
sclerosis,  progressive  locomotor  ataxia,  progressive  muscular  atrophy, 
labio-glosso-laryngeal  paralysis,  and  ophthalmoplegia  externa.  In  the 
brain  it  may  be  the  cause  of  acute  and  chronic  meningitis,  hemorrhage, 
thrombosis,  and  even  embolism  of  the  arteries;  thrombosis  of  one  of 
the  sinuses  in  cases  of  chronic  pachymeningitis ;  a  defined  gummatous 
growth;  and  a  chronic  degeneration  in  which  the  symptoms  are  very 
similar  to  those  of  general  paralysis  of  the  insane,  while  it  may  also  be 
the  direct  or  indirect  cause  of  functional  cerebral  lesions  like  epilepsy, 
hysteria,  and  chorea. 

Inherited  syphilis,  besides  giving  rise  to  various  local  diseases  in  the 
peripheral  nerves,  spinal  cord,  and  brain,  or  their  membranes,  is  often 
the  cause  of  imbecility  in  childhood,  which  progresses,  if  unchecked, 
until  the  mental  faculties  are  destroyed.  The  disease  appears  to  begin 
as  a  chronic  meningitis  of  the  convexity,  and  it  leads  to  a  progres- 
sive destruction  of  the  cortex  of  the  brain.  When  the  change  spreads 
over  the  motor  area  of  the  cortex  it  gives  rise  to  a  bilateral  sclerosis 
of  the  pyramidal  tracts,  and  corresponding  to  this  change  there  is, 
during  life,  a  spasmodic  paralysis  of  the  legs  first,  and  ultimately  of  all 
the  extremities.  The  growth  of  the  brain  may  also  be  arrested  by 
thickening  of  the  cranial  bones  from  syphilitic  osteitis,  or  from  narrow- 
ing of  the  arteries  from  syphilitic  endarteritis.  It  asserted  by  Virchow 
that  syphilis  is  sometimes  a  cause  of  congenital  myelitis  and  encepha- 
litis, and  hydrocephalus  appears  to  be  frequently  met  with  in  the  chil- 
dren of  syphilitic  parents. 

Nervous  affections  belong,  as  a  rule,  to  the  later  manifestations  of 
syphilis,  and  make  their  appearance  long  after  the  more  prominent  phe- 


PATHOLOGICAL    DIAGNOSIS.  707 

nomena  of  constitutional  syphilis  have  ceased  to  exist.  Search  must 
then  be  made  for  cicatrices  on  the  genitals  or  on  the  groins ;  circular 
pigmented  spots  on  the  skin ;  depressed  and  irregular  cicatrices  over 
the  forehead  and  front  of  the  legs,  with  the  integument  adhering  to  the 
subjacent  bones;  radiated  cicatrices  on  the  mucous  membranes,  especi- 
ally of  the  mouth ;  circular  depressions  on  the  arches  of  the  palate  or 
tonsils,  which  look  as  if  a  piece  of  tissue  had  been  punched  out ;  irregu- 
lar protuberances  on  the  surfaces  of  the  bones;  a  moderate  degree  of 
hard  swelling  of  the  occipital,  cervical,  or  cubital  lymphatic  glands; 
enlargement  and  knobby  induration  or  atrophy  of  one  testicle;  cicatrix 
on  the  penis ;  and  the  existence  of  iritic  adhesions.  An  inquiry  into 
the  history  of  a  case  may  throw  great  light  on  its  nature.  If  the  patient 
be  a  man,  it  may  be  asked  whether  lie  has  ever  suffered  from  syphilitic 
infection.  In  the  case  of  a  married  woman,  valuable  information  may  be 
obtained  by  ascertaining  whether  or  not  she  has  had  miscarriages,  if 
some  of  her  children  were  stillborn  or  died  soon  after  birth,  or  if  those 
living  manifest  any  of  the  characteristic  symptoms  of  congenital  syphilis. 
It  is  probable  that  nearly  one-half  of  the  cases  of  paralysis  of  the  third, 
fourth,  fifth,  and  sixth  nerves,  when  one  nerve  only  is  affected,  are  of 
syphilitic  origin,  and  curable  by  antisyphilitic  treatment.  The  paral- 
ysis of  the  ocular  nerves  which  occurs  in  the  course  of  locomotor  ataxia, 
is  likewise,  in  the  large  majority  of  cases,  an  indirect  result  of  syphilis. 
When  a  gummatous  deposit  takes  place  into  the  spinal  pia  mater,  or 
into  the  substance  of  the  spinal  cord,  the  clinical  features  of  the  case 
often  present  more  or  less  of  the  form  of  a  hemiparaplegia,  but  the 
symptoms  are  never  strictly  unilateral,  and  there  is  an  absence  of  the 
definite  phenomena  which  are  observed  on  a  level  with  the  upper  limit 
of  the  lesion  in  other  forms  of  spinal  tumor.  An  outburst  of  cerebral 
syphilis  is  often  preceded  for  tAvo,  three,  or  more  weeks,  by  a  deep- 
seated  headache,  with  intense  nocturnal  exacerbations  and  sleeplessness. 
If  a  person  after  suffering  from  a  headache  of  this  kind  is  attacked  with 
recurring  unilateral  convulsions,  each  of  which  is  followed  by  a  slight 
degree  of  paresis  of  the  muscles  affected  by  spasm,  the  case  is  one  of 
local  syphilitic  cerebral  meningitis  of  the  convexity,  either  primary  or 
secondary  to  disease  in  the  bones,  or  a  gummatous  growth  in  or  near 
the  cortex.  The  presence  of  double  optic  neuritis  in  such  a  case  points 
to  a  gimima  rather  than  meningitis.  An  apoplectic  attack  occurring 
before  forty-five  years  of  age  in  a  person  who  is  free  from  cardiac  or 
renal  disease,  points  strongly  to  syphilis,  thrombosis  if  tlie  attack  be 
slight,  or  hemorrhage  from  the  bursting  of  an  aneurism  if  it  assume 
the  form  of  ingravescent  apoplexy. 


708  GENERAL    DIAGNOSIS. 

The  manner  in  whieli  the  symptoms  are  associated  may  help  us  in 
recognizing  the  presence  of  syphilis  even  in  the  absence  of  other  evi- 
dence. Syphilitic  lesions  are,  as  Dr.  Broadbent  expresses  it,  often 
"multiple,  seldom  symmetrical."  Peripheral  paralysis  of  one  of  the 
ocular  motor  nerves  of  one  side  is  probably  never  associated  with  a 
similar  paralysis  of  the  corresponding  nerve  of  the  opposite  side,  but  is 
frequently  accompanied  by  a  unilateral  epilepsy,  or  by  a  hemiplegia  on 
one  or  other  side,  from  syphilitic  thromltosis.  Syphilitic  affections  of 
the  fifth  nerve  are  also  probably  never  bilateral,  and  if  both  of  these 
nerves  are  paralyzed  by  a  tumor  at  the  base  of  tlie  bi-ain,  the  growth  is 
likely  to  be  cancer.  The  succession  of  the  symptoms  may  also  aftbrd 
important  aid  in  diagnosis.  The  lesions  of  syphilis  being  multiple, 
appear  at  difteient  times  and  in  Avidely  different  j)arts  of  the  nervous 
system,  and  thus  a  grouj)  of  symptoms,  such  as  that  caused  by  paralysis 
of  a  cranial  nerve,  is  apt  to  be  followed  after  a  time  by  a  convulsion 
from  a  deposit  of  gummatous  tissue  on  the  surface  of  the  brain,  or  by 
hemiplegia  from  thrombosis  of  a  vessel.  In  nervous  affections  supposed 
to  result  from  inherited  syphilis,  it  is  imj)ortant  to  observe  the  general 
conformation  and  physiognomy  of  the  patient,  and  to  examine  the  long 
bones  for  evidence  of  periostitis,  and  the  fundus  of  the  eye  for  choroi- 
ditis disscminatd,  besides  making  minute  inquiries  into  the  family 
history. 


INDEX. 


*  BDOMINAL  reflex,  173 
A     Abducens  nerve,  paralysis  of,  363 

nerves,  spasm  of,  296 
Abscess  of  brain,  623 
Accelerated  breathing,  211 
Accessory  portions  of  the  nervous  system, 

83 
Achilles-tendon  reaction,  177 
Achromatopsia,  275 
Acoustic  nerves,  diseases  of,  269 
Acute  ascending  paralysis,  425 
atrophic  spinal  paralysis,  426 
pathology  of,  456 
atrophic  spinal  paralvsis  of  adults, 

482 
decubitus,  146 
hj'drocephalus,  653 
pysemic  encephalitis,  622 
^sthesioneuroses,  125 
articular,  131 
cutaneous,  126 
muscular,  130 
osseous,  131 
primar\',  125 
secondary,  125 
visceral,  132 
Agraphia,  638 

Akinesis  of  the  muscles  of  external  re- 
lation, 165 
of  the  deep  reflexes,  179 
of  the  superficial  reflexes,  176 
Albuminuric  neuritis,  278 
perineuritis,  278 
retinitis,  278 

degenerative,  278 
hemorrhagic,  278 
inflammatory,  278 
pathology  of,  279 
S3'mptoms  of,  279 
Alcoholic  paralysis,  415 
AUochiria,  127 
Alternate  hemiplegia,  477 
pathology  of,  495 
Amaurosis,  273 
Amblyopia,  273 
Amima,  639 
Amnesic  aphasia,  640 
Amyelia,  90 


Amyloid  corpuscles,  103 
Amyotrophic  lateral  sclerosis,  474 
Anaemia  of  the  brain,  603 

of  the  spinal  cord,  539 

patholog\'  of,  545 
treatment  of,  546 
Anaesthesia,  125 

in    region    of   the    distribution    of 
nerves,  243 

in    region    of    the    distribution     of 
plexuses,  243 

of  the  gustatory  nerves,  272 

of  the  mucous  membranes,  134 

of  the  olfactory  nerves,  268 

of  the  sexual  feelings,  134 

of  the  vagus,  134 
Ansesthesia?  dolorosa,  128 

muscular,  131 

visceral,  133 
Anal  neuralojia,  265 
Analgesia,  125,  128 

in   region  of  distribution  of  nerves 
and  plexuses,  243 

visceral,  133 
Anatomical  introduction,  17 
Anencephalia,  91 
Aneurism,  intracranial,  104 
Angina  pectoris,  207 

reflectoria,  209 
vaso-motoria,  209 
Angiomata,  108 
Angioneuroses,  216 

cerebral,  219 

peripheral,  218^ 

spinal,  218 

visceral,  220 
Angoraphobia,  139 
Anidrosis,  153 
Ankle-clonus,  177 
Anosmia,  268,  288 
Anterior  gray  horn,  44 

poliomyelitis,  426,  434 
pathology  of,  455 
treatment  of,  469 

pyramidal  tracts,  56 

root  zone,  48 
Anthrophobia,  139 
Aphasia,  192,  63*^ 


710 


INDEX. 


Aphasia,  amnesic,  640 

mixed,  643 

motor  or  ataxic,  638 

pathology  of,  644 

sensory  or  amnesic,  640 
Aphemia,  638 
Aphonia  paralytica,  877 
Aphthongia,  298 
Apncea,  211 
Apoplexy,  cerebral,  610 

treatment  of,  617 
Apselaphesia.  128 
Arachnitis,  574 
Argyll-Kobertson  pupil,  201 
Arteries,  21 

anterior  cerebral,  25 

branches  of,  80 
spinal,  21 

antero-lateral  cerebral,  group  of,  26 

antero-median  cerebral,  group  of,  26 

atheroma  of,  104 

basilar,  24 

central  system  of,  27 

choroid,  26 

circle  of  Willis,  25 

cortical,  25 

system  of,  26 

ganglionic  system  of,  27 

lenticulo-striate,  30 

middle  cerebral,  26 

branches  of,  30 

nutrient  of  medulla  and  pons,  24 

posterior  cerebral,  25 

branches  of,  30 
communicating,  26 
median  cerebral,  group  of,  25 
spinal,  21 

postero-lateral  cerebral,  group  of,  25 

spinal,  21 

nutrient,  22 

Sylvian,  26 

vertebral,  23 
Arthroneuralgia,  132 
Articular  iijsthesioneuroses,  131 
Articulation*,  disorders  of,  131 
Ascending  degeneration  of  the  nervous 

tissues,  113 
Aspermatism,  134 
Asphyxia,  212 

local,  of  llaynaud,  147 
Associated  movements  of  paralyzed  parts, 

183 
Asthma  nervosum,  212 
Ataxia,  jtrogressive  locomotor,  511 
Ataxic  gait,  522 
Atelomyelia,  90 
Atheroma,  104 
Athetosis,  481 

bilateral,  483 
Atrophic  paralysis,  356 
Atrophy  of  the  cerebellum,  630 

of  the  cerebral  hemispheres,  630 


Atrophy  of  the  corpus  callosum,  630 

of  the  face,  149 

of  the  nerves,  239 

of  the  optic  nerves,  281 

progressive  muscular,  437 
Attacks  of  sneezing,  310 

of  yawning,  311 
Audition,  loss  of,  288 
Auditory  hallucinations,  288 

hypera^sthesia,  269 

hyperalgesia,  269 

nerves,  diseases  of,  269 
Aura?  epilepticie,  328 
Aural  vertigo,  509 
Automatic  action,  65 

kinesioneuroses,  181 

movements,  160 
Azygos  uvula>,  paralysis  of,  373 


BASAL  ganglia,  53 
Basiilar  meningitis,  663 
13aths,  226 

brine,  226 

hot  air,  226 

hot  sand,  226 

mud,  226 

needle,  226 

shower,  226 

sponge,  226 

Turkish,  226 

vapor,  226 

warm,  226 
Bedsores,  146 
Bell's  paralysis,  365 
Bilateral  athetosis,  483 

facial  jiaralysis,  369 
Bladder,  nervous  disorders  of,  215 
Blepharospasm,  298 
Bloodletting  in  nervous  diseases,  227 
Bones,  nutritive  affections  of,  151 
Brachial    monospasms    or    protospasms, 
324 

plexus,  diseases  of,  306 
Brain,  91 

abscess  of,  623 

ansemia  of,  603 

atrt)phy  of,  630 

compression  of,  600 

concussion,  598 

congenital  malforn)ations  of,  91 

congestion  of,  608 

contusion  of,  599 

disease  of  membranes  of,  651 

hemorrhage  of,  610 

hypertropiiy  of,  631 

parasites  of,  108 

syphilis  of,  705 

tumors,  682 

unilateral  atrophy,  497 
Bulbar  mj-elilis,  552 

treatment  of,  566 


INDEX. 


711 


Bulbar  paralysis,  chronic  progressive,  442 

See  labioglosso-laryngeal  paralysis. 
Bulimia,  138 


CALCAREOUS  degeneration  of  nerve 
fibres,  102 
Carcinomata,  106 
Cardiac  nervous  mechanism,  20-5 
disorders  of,  207 
plexus,  neurosis  of,  263 
Cardialgia,  263 
Catalepsy,  342 

etiology  of,  342 
symptoms  of,  342 
treatment  of,  355 
Cataleptic  attacks,  338 
Causalgia,  127 
Central  galvanization,  233 
myelitis,  551 

pathology  of,  562 
treatment  of,  566 
Centrum  ovale,  30 
Cephalalgia,  584 
Cerebellar  diseases,  528 
Cerebello-spinal  conducting  path^,  63 
functions  of,  67 
system,  functions  of,  75 
Cerebral  abscess,  628 
aniemia,  603 
partial,  604 
treatment  of,  61G 
universal,  G03 
angioneuroses,  219 
apoplexy,  610 
concussion,  598 
congestion,  608 
convolutions,  relations  of,  to  skull, 

31 
embolism,  605 
facial  paralysis,  370 
hemorrhage,  610 

treatment  of,  617 
sinuses,  thrombosis  of,  606 
thrombosis,  005 
tumors,  632 
Cerebro-spinal  conducting  paths,  GO 
functions  of,  66 
multiple  sclerosis,  674 
system,  functions  of,  68 
Cervical   portion  of  the  cord,  lesions  of, 
203 
sympathetic,    depressive    lesions    of, 
202 
disorders  of,  202 
irritative  lesion  of,  202 
lesions  of,  204 
morbid  anatomy  of,  203 
physiology  of,  203 
Cervico-brachial  neuralgia,  253 
Cervico-occipital  neuralgia,  252 
Chasme,  311 


Cheyne-Stokes  respiration,  212 
Choked  disk,  277 
Cholesteatoma,  107 
Chorda  tympani,  lesions  of,  272 
Chorea,  679 
of  iris,  200 
of  the  larynx,  302 
pathology  of,  686 
post-hemiplegic,  480 
prehemiplegic,  480 
treatment  ol",  688 
Chromidrosis,  154 
Chronic  arthritis,  152 

atrophic  spinal  paralysis,  434 
decubitus,  147 
hydrocephalus,  658 
inflammation  of  nervous  tissues,  111 
progressive  bulbar  paralysis,  442 
Ciliary  muscle,  paralysis  of,  302 
Circle  of  Willis,  25 
Circumscribed  anesthesia,  128 
Cirrhosis  of  muscle,  141 
Classification  according  to  the  alterations 
of  function  produced  by  lesion,  96 
according  to  the  form  of  the  lesion, 

95 
of  lesions  of  nervous  system,  93 
Claustrophobia,  139 
Clinical  diagnosis,  090 
Clonic  spasms,  166,  481 
Clonus,  various  forms  of,  177 
Coccygeal  nerves,  neuralgia  of,  261 
Coccygodynia,  261 
Colica  saturnina,  268 
Colloid  bodies,  103 
Color  blindness,  275 
Columns  of  Clarke,  56 
of  Goll,  57,  68 
of  Tiirck,  56 
Combined  tonic  and  clonic  spasms,  479 
Compound  testhcsioneuroses,  185 
Compression  mj'elitis,  556 
pathology  of,  564 
treatment  of,  506 
of  the  brain,  600 
of  nervous  tissues,  95 
Compulsory  movements,  182 
Concussion  of  the  brain,  598 
treatment  of,  602 
of  the  spinal  cord,  596 
Congenital  defects  of  nerves,  90 
of  spinal  cord,  90 
malformations  of  the  skull  and  brain, 
91 
Congestion  of  the  brain,  608 
treatment  of,  617 
of  the  optic  nerves,  276 
of  the  nerves,  237 
treatment  of,  241 
Conjugate  deviation  of  the  eyes  and  ro- 
tation of  the  head  and  neck,  185 
Continuous  tremor,  481 


712 


INDEX. 


Contracture,  167 

myopathic,  167 

paralytic  or  secondary,  167 

primary  or  neuropathic,  167 
Contusion  of  the  brain,  699 
Convulsions,  internal,  299 
Convulsive  tic,  297 
Coordinate  cramps,  182 
Corpus  dentatum,  53 
Cortex  cerebelli,  53 

cerebri,  49 
Counter-irritation    in    nervous   diseases, 

227 
Cranial  reflexes,  175 
Cremasteric  reflex,  173 
Crises,  cardiac,  518 

tabetic  gastric,  518 
laryngeal,  517 
Crossed  hemiplegia,  477 
Crural  monospasms  or  protospasms,  324 

neuralgia,  250 
Crutch  paralj-sis,  391 
Cutaneous  ana;sthesia,  128 

eruptions  in  diseases  of  the  brain,  144 
in  diseases  of  the  spinal  cord,  144 
in  lesions  of  peripheral  nerves, 
143 

hemiana?sthesia,  288 

hyperoesthesire,  127 

hyperalgesia,  128 

pariBsthesiiP,  129 

paralgesia',  129 

trophic  affections,  143 
Cycloplegia,  363 
Cystalgia,  267 
Cystic  growths,  107 
Cysticercuscellulosa,  108 


DECUBITIS  acutus,  146 
chronic,  147 
Deep  reflexes,  176 
Defects  of  development,  90 
Degeneration     of    fillet     and     superior 
peduncle  of  the  cerebellum,  116 
of  the  nerves,  100 
of  the  nerve  centres  and  conducting 

paths,  120 
of  sensory  ganglia  and  conducting 
paths,  120 
Degenerative   albuminuric  retinitis  and 

perineuritis,  278 
Deiter's  cells,  103 
Delusion,  135 
Depressive  lesion  of  cervical  sympathetic. 

202 
Descending  degeneration  of  the  nervous 
tissues,  114 
optic  neuritis,  277 
Deviation,  secondary,  of  sound  eye,  189 
of  the  eyes  and  rotation  of  the  head 
and  neck,  185 


Diagnosis,  clinical,  690 
general,  690 
pathological,  699 
topographical,  691 
Diaphragmatic  paralysis,  385 
spasm,  305 

clonic,  306 
tonic,  305 
Diastematomyelia,  90 
Dill'used  atrophy  of  the  brain,  477 
Diphtheritic  paralysis,  418 
Diplegia  facialis,  369 
Diplomyelia,  90 
Dipsomania,  138 

Diseases  of  motor  coordination,  509 
of  the  acoustic  nerve,  269 
of  the  cerebellum,  528 
of  the  cerebrum,  603 
of  the  gustatory  nerves,  270 
of  the  membranes  of  the  brain,  651 
pathologj-  of,  667 
treatment  of,  669 
of  the  olfactory  nerve,  267 
of  the  optic  commissure  and  tracts, 

283 
of  the  optic  nerves,  273 
of  the  pia  mater,  653 
of  the  spinal  membranes,  669 
Disorders  of  common  sensation,  243 
of  special  sense,  243 
of  the  associated  movements  of  artic- 
ulation, 191 
of  the  associated  movements  of  the 

extremities,  190 
of  the  cardiac  accelerator  mechan- 
ism, 209 
of   the    cardio-inhibitory  centre  in 

medulla,  209 
of  the  cardio-inhibitory  mechanism, 

208 
of  the  inhibitory  fibres  of  the  vagus, 

208 
of  the  nerves  of  special  sense,  267 
of  the   nervous    mechanism    of  the 
bladder,  214 
of  the  heart,  205 
of  respiration,  210 
of  the  reflex-inhibitory  mechanism, 

209 
of  the  sense  of  smell,  288 
of  the  simple  reflex  cardiac  mechan- 
ism, 207 
of  the  visual  sense,  289 
Disseminated  myelitis,  561 

sclerosis,  674 
Dissolution  of  nerve  cells  and  fibres,  96 
of  the  nervous  system,  93 
law  of,  "93 
Dorso-intercostal  neuralgia,  254 
Double  consciousness,  137 
Dysesthesia,  127 
Dyschromatopsia,  275 


INDEX. 


718 


D3'Spliagia  paralytica,  t37C 
Dyspnoea,  211 


ECHINOCOCCUS  hominis,  108 
Eclampsia,  333 
asphyxic,  334 
etiology  <if,  334 
febrile,  334 
idiopathic,  384 
puerperal,  334 
reflex,  334 
symptoms  of,  334 
toxic,  334 
treatment  of,  353 
urtemic,  334 
Ecstasy,  344 

Electric  acupuncture,  232 
Electrical  reaction  of  afiected    muscles 
162 
of  nerves,  162 
Electricity,  231,  233 
Embolism,  104 

of  the  spinal  cord,  539 
Encephalitis,  620 

abscess  with,  623 
complicating  other  lesions,  623 
infantile,  621 
pathology  of,  628 
pyasmic,  622 

secondary  to  embolism,  627 
to  thrombosis,  627 
to  a  tumor,  628 
traumatic,  621 
treatment  of,  629 
Encephalic  automatic  disorders,  182 
Encephalo-spinal  conducting  paths,  54 
system,  49 

functions  of,  67 
Encephalocele,  92 
Encephalo-spino-neural  system,  21 
arteries  of,  21 
internal  structure  of,  41 
relation  of,  to  skeleton,  31 
topography  of,  31 
Engorged  disk,  277 
Enteralgia,  263 
Epigastric  reflex,  173 
Epilepsy,  327 
aursB,  328 

complications  of,  332 
etiology  of,  327 
grave,  330 
minor,  330 

morbid  anatomy  of,  348 
symptoms  of,  328 
treatment  of,  353 
varieties  of,  330 
Epileptic  mania,  333 
Epileptiform  neuralgia,  251 
Erect  posture,  78 
Erector  spinal  reflex,  173 


Erythemomegalalgia,  260 
Examination  of  the  body  during  move- 
ment, 159 

of  the  body  during  repose,  159 
External  cerebral  pachymeningitis,  651 

kinesioneuroses,  158 

remedies  in  nervous  diseases,  225 
Eyeballs,  paralysis  of  the  muscles  of,  359 
Eyelids,  disorders  of  the  movements  of 

the,  356  .   / 
Eyes,  conjugate  deviation  of  the,  185 

secondary  deviation  of  sound,  189 


IjiACIAL  atrophy,  149 
monospasm  or  protospasm,  325 
nerve,  paralysis  of,  370 
spasm  of,  297 
Fainting,  138 
Faradic  excitability,  161 
Faradization,  232 

general,  233 
Fascial  reactions,  177 
Femoral  neuralgia,  256 
Fibroma,  105 
Field  of  vision,  274 

alterations  in,  274 
diminution  in  acuteness  of,  274 
tests  of,  274 

acuteness  of,  274 
Fifth  nerve,  neuralgia  of,  245 
Fillet,  49 

degeneration  of,  116 
Forced  movements,  182 
Formation  of  a  nervous  system,  19 
of  nervous  constituents,  18 
of  nervous  tissues,  19 
Formatio  reticularis,  48,  58 
Formication,  129 
Fractures,  trophic,  152 
Functions  of  the    cerebello-spinal   con- 
ducting paths,  67 
system,  75 
of    the     cerebro-spinal     conducting 
paths,  66 
system,  68 
of  the  encephalo-spinal  system,  67 
I  Fundamental    portions   of    the    nervous 
system,  83 


GAIT,  ataxic,  522 
hemiplegic,  478 
spastic,  472 
Galvanic  excitability,  161 
Galvanization,  2^2 

central,  233 
Galvano-faradization,  233 
Ganglion  cells, 

atrophy  of,  99 

calcareous  degeneration  of,  99 

colloid  degeneration  of,  99 


714 


INDEX. 


Ganglion  cells,  hypertrophy  of,  96 

multiplication    of    the    nucleus 

and  nucleolus  in,  97 
pigmentary  de«ceneration  of,  99 
shrinking  of,  97 
vacuo lation  of,  99 
Gangrene,  symmetrical,  147 
Gastralgia,  263 
Gastric  crises,  tabetic,  518 
Gastrodynia,  263 
General  diagnosis,  690 

diseases  of  the  perijiheral  nerves,  237 
faradization,  233 

morbid  anatomy  and  physiology,  122 
of  the  nervous  system, 
90 
myopathic  spasms,  321 
symptomatology,  125 
treatment  of  nervous  disea:<es,  222 
medicinal,  223 
prophylactic,  222 
Genital  organs,  nervous  disorders  of,  215 
Giant  cells,  51 
Girdle  anicsthesia,  128 

sensation,  127 
Glaucoma,  151 
Gliomata,  106 
Globus,  133 
Glossoplegia,  371 
Glossy  skin,  143 
Gliige's  corpuscle.',  103 
Gluteal  reflex,  173 
Grapliospasmus,  308 
Gray  degeneration  of  the  posterior  col- 
umn, 511 
softening,  110 

substance  of  tlie  cerebellum,  53 
of  cerebrum,  49 
Green  softening,  110 
Gustatory  nerves,  anivsthesia  of,  272 
diseases  of,  270 
hyperipsthesia  of,  272 
Gynephobia,  139 


H.EMATIDROSIS,  154 
Haematoma  of  the  dura  mater,  651 
Htematomyelia,  541 
Hamiatorrhachis,  569 
Hair,  trophic  changes  in,  145 
Hallucination,  135 

of  hearing,  289 

of  sight,  289 

of  the  sense  of  smell,  288 
Headache,  137,  584 

anaemic,  584 

congestive,  584 

gouty,  585 

hyperiemic,  584 

hysterical,  584 

neurasthenic,  585 

organic,  586 


Headache,  pyrexia),  585 

rheumatic,  585 

sick,  586 

sympathetic,  585 

syphilitic,  585 

toxic,  584 

treatment,  591 
Hearing,  disorders  of,  289 
Heart,  nervous   mechanism   of,   and    its 

disorders,  205 
Hemeralopia,  275 
Hemian:osthesia,  crossed,  128,  286 

cutaneous,  288 

muscular,  288 
Hemianopsia,  283,  284 

crossed,  284 

double  nasal,  284 
temporal,  284 

equilateral,  284 

homonymous,  284 
Hemiataxia,  481 

Uemiatrophia  facialis  progressiva,  149 
Hemicephalia,  91 
Hemicrania,  91.  586 

pathology  of,  589 
Heiniparanicsthesia,  285 
Heniiparaplegia,  557 
Hemiplegia,  })athology  of,  476,  491 

and  iiemiana'sthcsia,  477 
pathology  of,  493 

facialis,  365 

from  cortical  disease,  505 

liemianaistliesia,   and    hemianopsia, 
477 
pathology  of,  493 
Hemiplegia^,  spastic,  of  infancy,  482 
Hemiplegic  gait,  478 
Hemorrhage,  cerebral,  610 

into  the  S|)inal  cord,  541 
pathology  of,  546 
Hemorrhagic  alliuminuric  retinitis   and 

perineuritis,  278 
Hepatalgia,  264 
Herpes  zoster,  143 
Heteroto|tia  of  brain  substance,  631 
Hiccough,  306 
Hippus,  200 
Histrionic  chasm,  297 
Homonymous  hemianopsia,  284 
Hydrencephalocele,  92 
Hydrocephalus,  acute,  653 

chronic,  658 
Hydromyelia,  436 
Hydromyelus  congenitus,  91 
Hydrorrhachis  interna,  91 
Hyperacusia,  269 
Hyperaemia  of  brain,  608 

of  the  nerves,  237 

of  the  spinal  cord,  540 

pathology  of,  545 
treatment  of,  546 

of  the  spinal  membranes,  569 


INDEX. 


715 


Hyperesthesia,  125 

in  region  of  distribution  of  nerves 
and  plexuses,  244 

muscular,  130 

of  the  auditory  nerve,  269 

of  the  gustatory  nerves,  272 

of  the  olfactory  nerve,  208 

of  the  ovary,  260 
Hyperifisthetic  spots,  127 
Hyperalgesia,  125 

in  region  of  distribution  of  nerves 
and  plexuses,  244 

muscular,  130 

of  the  sense  of  smell,  268 

visceral,  132 
Hyperidiosis,  153 

unilateralis,  154 
Hyperkineses  of  the  deep  reflexes,  179 

of  the  muscles  of  external  relation, 
165 

of  the  superficial  reflexes,  175 
Hyperosmia,  268 

Hyperplasia  of  the  Pineal  gland,  106 
Hyporpselaphesia,  127 
Hypertrophy  of  axis-cylinder,  102 

of  the  brain,  631 

of  the  nerves,  240 
Hypnotism,  844 
Hypogastric  neuralgia,  265 
Hypoglossal  nerve,  paralysis  of,  371 
Hysteralgia,  265 
Hysteria  in  boys,  338 
Hysterical  attacks,  337 

treatment  of,  353 

paralysis,  486' 

spasmodic  affections,  836 

morbid  anotomy  of,  349 
Hystero-epilepsy,  340 


TLLUSION,  135 
±     Impotency,  134 
Infantile  paralysis,  427 

spinal  atrophic  paralysis,  427 
atrophy,  429 

deforinity  of,  429 
invasion  of,  427 
regression  of,  428 
remission  of,  427 
Inflammation  of  the  nerves,  237 
treatment  of,  241 
of  the  spinal  dura  mater,  570 
of  the  spinal  pia  mater  and  arach- 
noid, 574 
Inframaxillary,  249 
Insular  sclerosis  of  brain  and  cord,  671 
Intercentral  connections,  73 
Intermediate  cerebral  ganglia,  53 

ganglia    of    the    cerebello-spinal 
S3'stem,  63 
Internal  cerebral  pachymeningitis,  651 
Intestinal  colic,  263 


Intracranial  tumors,  632 
pathology  of,  634 
treatment  of,  635 
Iridoplegia,  200 
Iris,  chorea  of,  200 

disorders  of  movement  of,  198 
nervous  mechanism  of,  197 
Irritative  lesion  of  cervical  sympathetic, 
202  J     F  . 


J 


OINTS,  nutritive  affections  of,  151 


KINESIONEUKOSES,  176 
automatic,  181 
classification  of,  168 
clinical,  169 
etiological,  168 
pathological,  168 
topographical,  168 
elementary,  158 
external,  158 
reflex  central,  173 
vascular,  210 
visceral,  194 
Knee-jerk,  170 
Knee-phenomenon,  176 


T  ABIO-GLOSSO-LARYNGEAL 
Jj     paralysis,  442 

pathology  of,  503 
Labyrinthine  vertigo,  509 
Landry's  paralysis,  425 
Larj'ngeal  crises,  301,  517 

disorders,  301 
Laryngismus  stridulus,  299 
Lateral  pj'ramidal  tracts,  56 

sclerosis,  528 
Layers  of  the  cortex,  50 
Lead  colic,  414 

paralysis,  413 
Lenticulo-striate  artery.  30 
Leptomeningitis  spinalis  acuta,  574 

chronica,  575 
Lesions  of  the  cervical   poi'tion  of   the 
cord,  203 

of  the  medulla  oblongata,  203 

of  the  rami  communicantL'S,  204 
Lightning-like  pains,  130 
Lingual  spasm,  298 
Lipoma,  107 
Local  asphyxia,  147 

hysterical  spasms,  338 

myopathic  spasms,  321 

spasms,  295 
Locomotor  ataxia,  511 

affections  of  special   senses   in, 

515 
anosmia  in,  516 


716 


INDEX. 


Locomotor  ataxia,  apoplectiform  attacks 
in,  520 
Argyll-Kobertson  pupil  in,  517 
ataxia  of  facial  muscles  in,  517 
ataxic  stage  of,  521 

sensory    disorders     in, 

524 
trophic  disorders  in,  526 
visceral    disorders    in, 
525 
bladder  affections  in,  518 
bone  affections  in,  520 
cardiac  crises  in,  518 
cerebral  disorders  in,  520 
deafness  in,  516 
disorders  of  the  pupils  in,  517 
epileptiform  attacks  in,  520 
etiology  of,  511 
facial  paralysis  in,  517 
gait  in,  522 
gastric  crises  in,  518 
hemiopia  in,  516 
joint  affections  in,  520 
laryngeal  crises  in,  517 
loss  of  taste  in,  516 
nephralgia  attacks  in,  518 
nystagmus,  517 

paralysisof  ocular  muscles  in, 51 6 
paralytic  stage  of,  526 
pathology  of,  531 
preataxic  stage,  512 
psychical  disorders  in,  520 
rectal  affections  in,  518 
symptoms  of,  511 
treatment  of,  536 
trigeminal  neuralgia  in,  517 
trophic  affections  in,  519 
varieties  of,  526 

anomalous,  527 

hemiataxic,  527 

hereditary,  527 

meningitic,  527 

neuralgic,  527 

paraplegic,  527 

typical,  526 
vaso-niotor  disorders  in,  519 
vesical  affections  in,  518 
Lordosis,  431 

Lumbo-abdominHl  neuralgia,  256 
Lumbar  neuralgia,  255 


MAINE  en  griffe,  396 
Massage,  227 
Massive  hemorrhages,  108 
Masticatory  monospasms  or  protospasms, 
327 
paralysis,  363 

diagnosis  of,  364 
etiology  of,  363 
symptoms  of,  363 
spasms,  296 


Mastodynia,  255 
Mechanical  vibrations,  230 
Median  nerves,  paralysis  of,  394 
Medulla  oblongata,  lesions  of,  203 
Melanoma,  107 
Meniere's  disease,  509 

etiology  of,  509 
pathology  of,  531,  533 
symptoms  of,  509 
treatment  of,  536 
Meningeal  apoplex}^  cerebral,  615 
spinal,  569 
hemorrhage,  cerebral,  615 
treatment  of,  617 
spinal,  569 

treatment  of,  577 
Meningitis,  basilar,  663 
metastatic,  664 

of  the  convexity  of  the  brain,  660 
rheumatic,  665 
simple,  663 
traumatic,  665 
tubercular,  653 
with  pneumonia,  665 
with  ulcerative  endocarditis,  665 
Meningo-myelitis,  560 
Mesenteric  neuralgia,  263 
Metastatic  meningitis,  664 
Methods   of  examining    the   motor   ap- 
paratus, 158 
Microcephalus,  92 
Microscopical  changes  in   inflammation 

of  nervous  tissues,  110 
Migraine,  586 
Mimetic  paralysis,  365 
Mimic  convulsion,  297 
Mixed  aphasia,  643 
Mogigraphia,  308 
Monojilegia,  485 

pathology  of,  499 
Monospasm,  323 
bracliiai,  324 

pathology  of,  500 
crural,  324 

pathology  of,  500 
facial,  325 

pathology  of,  502 
masticatory,  327 
oculo-motor,  326 
Motor  aphasia,  638 

cortical  centres,  71 
Motorium  commune,  73 
Morbid  anatomy  and  physiology  of  the 

atrophic  paralyses,  451 
Multiple  neural  paralyses,  412 

sclerosis  of  the  brain  and  cord,  674 
pathology  of,  684,  686 
treatment  of,  688 
Muscular  £Bsthesioneuroses,  130 
anaesthesia,  131 
atrophy,  progressive,  437 

with  nuclear  proliferation,  141 


INDEX, 


717 


Muscular  cirrhosis,  141 
hemiansesthesia,  288 
hyperaesthesia,  130 
hyperalgesia,  130 
sense,  131 
sensibility,  131 
tension,  167 
trophoneuroses,  140 
Musculo-spiral  nerve,  paralysis  of,  391 
Myalgia,  130 
Mydriasis,  199 
paralytic,  199 
spastic,  199 
Myelitis,  547 

etiology  of,  547 
pathology  of,  561 
symptoms  of,  548 
treatment  of,  565 
varieties  of,  551 
acute,  551 

pathology  of,  561 
bulbar,  552 
central,  551 
compressive,  556 
disseminated,  561 
meningo-,  560 
periependymal,  436 
transverse,  552 
traumatic,  554 
unilateral,  557 
universal,  560 
Myelomalacia,  539 
Myoneuralgia,  130 
Myopathic  spasms,  321 
etiology  of,  321 
pathology  of,  847 
svmptoms  of,  321 
Myosis,  198 

paralytic,  199 
spastic,  199 
3Iyxomata,  106 


NAILS,  trophic  changes  in,  145 
Xerve,  abducens,  paralysis  of,  363 
diseases  of  pneumogastric,  299 
Xerves,  anaesthesia  in  region  of  distri- 
bution of,  243 
analgesia  in  region  of  distribution 

of,  243 
atrophy  of,  239 
congenital  defects  of,  90 
congestion  of,  237 
degeneration  of,  101 
general  diseases  of,  237 
hypenemia  of,  237 
hyperfesthesia  of,  244 
hyperalgesia  of,  244 
hypertrophy  of,  240 
inflammation  of,  237 
regeneration  of,  100 


Nerves,  stretching  of,  235 
Nervous  asthma,  212 

constituents,  formation  of,  18 
disorders  of  the  bladder,  214 

of  the  genital  organs,  215 
exhaustion,  579 

mechanism     of    the     bladder     and 
rectum,  213 

of  the  genital  organs,  215 

of  the  iris,  197 
system,  anaemia  of,  94 

classification  of  lesions  of,  93 

degenerations  of,  94,112 

dissolution  of,  93 

embolism  of,  94 

formation  of  an,  19 

hemorrhage,  94,  108 

hyperemia  of,  94 

inflammation  of,  93,  109 

syphilis  of,  705 

thrombosis,  94 

toxic  lesions  of,  94 

traumatic  injuries  of,  94 

vascular  lesions  in,  94 
tissues,   ascending   degeneration   of, 
113 

capillary  extravasations  in,  104 

chronic  inflammation  of,  111 

compression  of,  95 

degenerations  of,  112 

descending  degeneration  of,  114 

dissolution  of,  102 

formation  of,  19 

hypertrophy  and  hyperplasia  of 
neuroglia  and  connective 
tissues  of,  103 

interstitial  sclerosis,  108 

microscopical  changes  in  acute 
inflammation  of,  110 

primary,  112 

secondarv,  113 
Neuralgia,  125,  129,  244 
anal,  265 
cervico-brachial,  258 

etiology  of,  253 

symptoms  of,  253 
cervico-occipital,  252 

etiology  of,  252 

symptoms  of,  252 

treatment  of,  252 
coccygodynia,  261 
cceliaca,  268 
cystic,  267 

dorso-intercostal,  254 
epileptiform,  251 
facial,  251 
femoral,  256 
gastric,  263 
hepatic,  264 
hypogastric,  265 
inframaxillary,  249 


718 


INDEX. 


Neuralgia  in  the  region  of  distribution 
of  nerves  and  plexuses,  245 
ischiadica,  257 
lumbar,  255 

femoral,  25G 

genital,  257 

liimbo-abdominal,  256 
mastodynia,  255 
mesenteric,  268 
muscular,  130 
oesophageal,  262 
of  mons  veneris,  257 
of  the  bladder,  267 
of  the  clitoris,  257 
of  the  fifth  nerve,  245 
of  the  penis,  257 
of  the  urethra,  267 
ophthalmic,  247 
ovarian,  266 
phar3^ngeal,  262 
phrenic,  252 
plantar,  260 

diagnosis  of,  262 

etiology  of,  260 

symptoms  of,  260 

treatment  of,  294 
sciatic,  257 

diagnosis  of,  262 

etiology  of,  257 

symptoms  of,  258 

treatment  of,  293 
supraorbital,  247 
supramaxiHary,  249 
testicular,  266 
trigeminal,  245 

etiology  of,  245 

symptoms  of,  245 

varieties  of,  247 

epileptiform,  251 
inframaxiliary,  251 
ophlhalmic,  247 
sup-amaxillary,  249 
supraorbital,  247 
treatment  of,  291 
urethral,  267 
uterine,  265 
Neuralgiform  pains,  129 
Neurasthenia,  579 
cerebral,  579 
etiology  of,  579 
spinal,  579 
symptoms  of,  579 
treatment  of,  591 
Neurectomy,  235 
Neuritis,  acute,  237 

chronic,  112 
Neuromata,  240 

etiology  of,  240 
false,  Y05 

motor  disorders  in,  240 
symptoms  of,  240 


Neuromata,  treatment  of,  242 

true,  105 
Neuroparalytic  ophthalmia,  150 
Neuropathic  constitution,  92 

paralyses,  171 
Neuro-retinitis,  277 
Neurotic  constitution,  92 
Neurotomy,  235 
Nictitating  spasm,  297 
Ninth  nerve,  paralysis  of,  371 
Notencephalus,  91 
Nutritive    affections    of    the    glandular 

apparatus,  153 
Nyctalopia,  275 
Nystagmus,  296 


OBTURATOR  neuralgia,  257 
paralysis,  405 
Occlusion  of  cerebral  capillaries,  608 
Oculo-motor  monospasm  or  protospasm, 
32G 
paralysis,  356 

symptoms  of,  360 
OEsophagcal  neuralgia,  262 
paralysis,  376 
spasm,  299 
ffisophagisnius,  299 
Olfactory  nerve,  ana)sthesia  of,  268 
diseases  of,  267 
hyperajsthesia  of,  268 
morbid  anatomy  of,  269 
physioloiry  of,  269 
Olivary  bodies,  54 
Operculum,  86 
Opisthotonos,  311 
Ophthalmia,  neuroparalytic,  150 
Ophthalmic  neuralgia,  247 
Ophthalmoplegia  externa  vel  progressiva, 
447 
pathology  of,  463 
interna,  200 
Optic  ana-thesia,  273 
hj'penesthoia,  273 
hyperalgesia,  273 
nerves,  aiia'.<thesia  of,  273 
congestion  of,  276 
diseases  of,  273,  276 
hyperesthesia  of,  273 
hyperalgesia  of,  273 
inflammation  of,  276 
primarv  and  secondary  atrophy 
of,  276,  281,  283 
neuritis,  277 
Ordinarv  hemi|)legia,  476 
Oscedo,  311 
Osmidrosis,  154 

Osseous    affections    of   cerebral    origin, 
152 
lesions  in  the  insane,  153 
('steomata,  107 


^ 


INDEX. 


19 


Osteoneuralgia,  131 
Ovarian  neuralgia,  266 


PACHYMENINGITIScerebralis,6.51 
external,  651 
internal,  651 

interna  hemorrhagica  spinalis,  573 
treatment  of,  577 
hypertrophica  spinalis,  571 
treatment  of,  577 
spinalis  externa,  570 

treatment  of,  577 
Painful  points,  130 
Palate,  paralysis  of,  373 
Palmar  reflex,  175 
Papilloma,  107 
Paradoxical  contraction,  178 
Parsesthesia?,  125 
visceral,  132 
Paralgesia?,  visceral,  133 
Paralysis,  356 

acute  ascending,  425 

acute  atrophic  spinal,  in  adults,  432 

in  children,  426 
agitans,  670 
alcoholic,  415 
Bell's,  365 
cerebral  facial,  370 
chronic  atrophic  spinal,  434 
progressive  bulbar,  442 
diphtheritic,  418 
from  functional  disease,  485 
hemiplegic,  476 
hypoglossal,  371 
hysterical,  484 
in  locomotor  ataxia,  526 
labio-glosso-laryngeal,  442 
Landry's,  425 
lead,  413 

levator  palati,  378 
masticatory,  363 
myopathic  atrophic,  448 
oculo-motor,  356 
of  ciliary  muscles,  363 
of  the  abdiicens,  363 
of  the  diaphragm,  385 
of    the    muscles    supplied    by    the 
brachial  plexus,  389 
by  the  cervical  plexus,  385 
by  the  dorsal  nerves,  402 
by  the  hypoglossal,  371 
by  the  hmibar  plexus,  403 
by  the  median  nerve,  394 
by  the  sacral  plexus,  408 
of  the  cesophagus,  376 
of  the  pharynx,  376 
of  the  respiratory  muscles,  402 
of  the  sixth  nerve,  363 
of  palate,  373 
peripheral  facial,  370 


Paralysis,  phonetic  laryngeal,  381 

pneumogastric,  373 

post-epileptic,  485 

primary  labio-glosso-laryngeal,  442 

pseudo-hypertrophic,  448 

reflex  atrophic,  422 

spasmodic,  471 

spinal  accessory,  383 
atrophic,  425 

toxic,  488 
Paralytic  mydriasis,  199 

myosis,  199 
Paranesthesia,  128,  284 
Paraplegiie,  471,489 

pathology  of,  490 
Parasites  of  the  brain,  108 
Parencephalus,  92,  497 
Paridrosis,  154 
Partial  aniesthesia,  128 

hypertrophy  of  brain,  631 
Patellar-tendon  reaction,  176 
Pathological  diagnosis,  699 
Perforating  ulcer  of  the  foot,  147 
Periependymal  myelitis,  436 

pathology  of,  457 
Perimeningitis,  570 
Perimyelitis,  574 
Perineuritis,  112,237 
Periodic  amnesia,  137 
Periosteal  reactions,  177 
Peripachymeningitis  spinalis,  670 
Peripheral  angioneuroses,  218 

automatic  disorders,  181 

of  the  larynx,  377 

facial  paralysis,  370 
Perverted  sexual  instinct,  138 
Pharyngeal  neuralgia,  262 
Phrenic  neuralgia,  252 
Physiological  introduction,  64 
Physiology  of  the  spas-modic  paralyses, 

506 
Piano-forte  player's  spasm,  310 
Pineal  gland,  hyperplasia  of,  106 
Plantar  neuralgia,  260 

reflex,  173 
Pleurosthotonos,  311 
Pneumogastric  nerve,  diseases  of,  299, 377 
Podynia,  262 
Points  apophysaire,  130 

douloureux,  130 
Poliencephalitis  acuta  infantium,  621 
Poliomyelitis  anterior  acuta,  426 

chronica,  434 
Poliomyelopathies,  425 
Polyaosthesia,  127 
Polydipsia,  133 
Post-epileptic  paralysis,  485 
Posterior  gray  horn,  46 

longitudinal  fasciculus,  48 

root  zone, 48 

sclerosis,  511 


720 


INDEX. 


Postero-median  columns,  57 
Post-hemiplegic  spasms,  478,482 
Pressure-arresting  points,  167 
Pressure- exciting  points,  167 
Primary  assthesioneuroses,  125 
areas  of  si<ull,  33 
degeneration  of  the  nervous  tissues, 

112 
labio-glosso-laryngeal  paralysis,  442 
lateral  sclerosis,  471 
sclerosis    of    the  columns    of    G^ll, 
510 
Professional  hyperkineses,  308 
Progressive  bulbar  paralysis,  442 
pathology  of,  462 
locomotor  ataxia,  511 
muscular  atrof)hy,  437 

treatment  of,  459 
pathology  of,  4(i4 
Prosopalgia,  365 
Pruritus,  129 
Protospasms,  328 
brachial,  324 

pathology  of,  500 
crural,  324 

pathology  of,  500 
facial,  325 

pathology  of,  502 
masticatory,  327 
oculo-motor,  326 
Psammomum,  107 
Pseudo-ajsthesia,  135 
Pseudo-hypertrophic  paralysis,  448 

pathology  of,  465 
Psychical  blindness,  290 

deafness,  289 
Puj)il,  Argyll-Robertson,  201 
Pupil,  reflex  immobility  of,  201 
Pyramidal  giant  cell,  51 
tract,  60 

sclerosis  of,  114 
Pyrosis,  133 


REACTION  of  degeneration,  164 
*Ked  softening,  109 
Reflex  action,  65 
akinesis,  173 
atrophic  paralj'sis,  422 
etiology  of,  422 
symptoms  of,  422 
central  kinesioneuroses,  173 
Reflexes,  abdominal,  173 
akineses  of  the  deep,  179 
cranial,  175 
cremasteric,  173 
deep,  176 
epigastric,  173 
erector  spinal,  173 
*  fascial,  177 

gluteal,  173 
hyperkineses  of  the  deep,  179 


Reflexes,  palmar,  175 
periosteal,  177 
plantar,  173 
scapular,  175 
Reflex  hyperkinesis,  173 

immobility  of  the  pupil,  201 
movements,  160 
spasms,  167 
Regeneration  of  nerves,  100 
Relation  of  cerebral  convolution  to  skull, 

31 
Relative  immunity  of  some  muscles  from 
paralysis,  184 
liability  of  some  muscles  to  convul- 
sions, 184 
Remittent  tremor,  481 
Respiration,  Cheyne-Stokes,  212 
Respiratory    nervous    mechanism,    dis- 
orders of,  210 
Retrobulbar    neuritis    and   perineuritis, 

278 
Rupture  of  the  brachial  plexus,  399 


SACRAL  plexus,  disorders  of,  257 
Saint  Vitus 's  dance,  679 
Saltatory  spasm,  313 

morbid  anatomy  of,  346 
Sarcomata,  107 
Scapular  reflex,  175 
Sciatica,  257 

Sclerosis,  amyotrophic  lateral,  474 
cerebro-spinal,  674 
disseminated,  674 
insular,  674 
multiple,  674 
of  the  posterior  and  lateral  columns, 

528 
of  the  posterior  columns,  511 
of  the  pyramidal  tracts,  114 
primary  lateral,  471 
primary,  of  columns  of  Goll,  510 
secondary,  of  columns  of  Goll,  511 
of  direct  cerebellar  tracts,  511 
lateral,  476 
Scotomata,  274 
Seclusion   in   the  treatment  of  nervous 

diseases,  227 
Secondary  ajsthesioneuroses,  125 
areas  of,  33 
degeneration  of  the  nervous  tissues, 

113 
deviation  of  the  sound  eye,  189 
lateral  sclerosis,  476 
sclerosis  of  the  columns  of  Goll,  511 
Secretory  functions,  66 

affections   of    glandular   apparatus, 

153 
disorders  of  the  glands  of  the  diges- 
tive tract,  156 
of   the   genito-urinary   ap- 
paratus, 156 


INDEX, 


721 


Secretory   disorders    of    the    lachrymal  I  Spasms  of  the  glottis  in  adults,  300 


;lands,  155 
of  the  salivary  glands,  ISi 
Segmental  periaxillary  neuritis,  112 
Sense  of  locality,  126 

of  pressure,  126 

of  temperature,  126 
Sensorium  commune,  73 
Sensory  aphasia,  640 

conducting  paths,  02 

cortical  centres,  70 

disorders  of  the  special  senses,  134 
Shock,  594 

erethismic,  595 

pathology  of,  601 

torpid,  594 

treatment  of,  G02 
Shoemakers'  spasm,  310 
Sick  headache,  586 
Simple  basilar  meningitis,  663 

glaucoma,  151 

muscular  atroph}^,  140 
Singultus,  o06 
Sixth  nerve,  paralysis  of,  363 

spasm  of,  296 
Skull,  primary  areas  of,  33 

secondary  areas  of,  33 
Smell,  disorders  of,  288 

hallucinations  of,  288 

hyperalgesia  of,  269 

illusions  of,  269 

loss  of,  288 
Sneezing,  attacks  of,  310 
Soft  palate,  paralysis  df,  373 
Solitary  tubercle,  106 
Somnambulism,  344 
Spasmodic  atiections  of  the  larynx,  299 

cough, 311 

disorders,  295  . 

gait,  472 

laryngeal  cough,  301 

spinal  paralysis,  471 

paralysis  of  infancy,  484 
Spasms,  165,  295 

cerebro-spinal,  323 

clonic,  160 

from  organic  disease  of  the  cortex 
of  the  brain,  323 

general  myopathic,  321 

hemiplegic,  478 

pathology  of,  496 

histrionic,  297 

hysterical,  337 

in  area  of  distribution  of  the  facial 
nerve,  297 

inspiratory,  310 

lingual,  298 

local  myopathic,  321 

masticatory,  296 

mimic,  297 

of  the  abducens  nerve,  296  . 

of  the  diaphragm,  305 


in  children,  299 
of  the  laryngeal  muscles,  302 
of  the  muscles  of  the  eyeball,  295 
of  the  neck,  305 
of  the  upper  extremity,  307 
sui)plied     by    the     hypoglossal 

nerve,  298 
supplied    by    the   lumbar    :ind 
sacral  nerves,  312 
by  the  sciatic  nerves,  312 
by  the  vagus  and  pharyn- 
geal plexus,  299 
of  the  obliquus  capitis  inferior,  305 
of  the  oesophagus,  299 
of  the  respiratory  muscles,  310 
of  the  sixth  nerve,  296 
of  the  soft  palate,  299 
of  the  splenius  capitis,  305 
of  the  trapezius,  302 
of  the  vocal  cords,  301 
piano-forte  players',  310 
post-hemiplegic,  478 
saltatory,  313 
shoemakers',    310 
tailors',  310 
telegraphers',  310 
tonic,  166 
toxic,  478 

and  clonic,  479 
Spastic  gait,  478 

hemiplegia  of  infancy,  482 
mydriasis,  199 
myosis,  199 
walk,  472,  478 
Special  pathology  of  the  nervous  system, 

237 
Spina  bifida,  91 

Spinal  accessory,  paralysis  of,  383 
angioneuroses,  218 
atrophic  paralysis,  425 
automatic  disorders,  182 
concussion,  596 

treatment  of,  602 
cord,  anajmia  of,  539 
apoplexy,  541 
concussion  of,  596 
congenital  defects  of,  90 
embolism  of,  539 
hemiplegia  of,  557   ' 
hemorrhage  of,  541 
hypenemia  in,  540 
irritation  of,  578 
relations  of  vertebra)  to,  31 
syphilis  of,  705 
thrombosis  of,  539 
tumors  of,  564 
epilepsy,  178 
irritation,  578 
Spino-neural  spasms,  295 
Splenius  capitis,  spasms  of,  30") 
Status  epilepticus,  333,  341 


46 


722 


INDEX. 


Slernutatio  convulsiva,  310 

Strabismus,  362 

Stretching  of  nerves,  235 

St.  Vitus's  dance,  679 

Subconscious  and  semiconscious  psych 

cal  actions,  136 
Superticial  reflex,  173 
Superior  peduncle  of  cerebellum,  116 
Supramaxillary  neuralgia,  249 
Supraorbital  neuralgia,  247 
Surface  of  skull,  landmarks  on,  31 

topography  of,  31 
Swedish  gymnastics,  230 
Symmetrical  gangrene,  147 
Synkinesis,  ltt3 
Syphilis  of  the  brain,  705 

of  the  cord,  705 

of  the  nervous  system,  705 
Syphilomala,  107 
Syringomyelia,  436 


T 


ABES   dorsalis,   511.     See   locomotor 
ataxia, 
spasmodic,  471 
Tabetic  amauroses,  281 

ecchymoses,  219 

foot,  152 

gastric  crises,  518 

laryngeal  crises,  301 
Tactile  anjesthesia,  128 
Tailors'  spasm,  310 
Teeth,  nutritive  attections  of,  151 

trophic  aliections  of,  153 
Telegraphers'  cramp,  310 
Tendon  reactions,  176 
Tenth  nerve,  diseases  of,  299,  377 
Testicular  neuralgia,  266 
Testis,  irritable,  266 
Tetanilla,  318 
Tetanus,  313 

etiology  of,  313 

morbid  anatomy  of,  346 

symptoms  of,  314 

treatment  of,  352 
Tetany,  318 

etiology  of,  318 

morbid  anatomy  of,  347 

symptoms  of,  319 

treatment  of,  352 
Thermo-ana2Sthesia,  128 
Thermo-hyperajsthesia,  127 
Thermo-hyperalgesia,  128 
Third  nerve,  monospasm  or  protospasm 
of,  326 
paralysis  of,  356 
Thomsen's  disease,  321     ^^  \ 
Thrombosis,  104 

of  the  cerebral  sinuses,  606 

of  the  spinal  cord,  539 
Tic,  convulsive,  297 

douloureaux,  245 


Tinnitus  aurium,  509 
Titillation,  183 
Toe  clonus,  177 
Tonic  and  clonic  spasms,  479 
spasms,  166,  478 

early  rigidity  in,  478 
lalerigidity  in,  47? 
T<^pographical  diagnosis,  691 
Topography  of    external  surface  of  the 

skull,  31 
Torticollis,  302 
Total  anaesthesia,  128 
Toxic  paralyses,  488 
Trance,  344 

Transverse  myelitis,  552 
pathology  of,  562 
treatment  of,  566 
Trapezius,  spasm  of,  302 
Traumatic  local  encephalitis,  621 
meningitis,  665 
myelitis,  554 

treatment  of,  566  . 
Treatment  of  the   spasmodic   paralyses, 

508 
Trigeminal  neuralgia,  245 
Trismus,  296 
Trophic  attections  of  the  teeth,  153 

disorders  of  the  nails  and   hair   in 
cerebral     affections, 
146 
in     lesions   of    nerve- 
trunks,  145 
in  spinal  disease,  145 
functions  of  the  cord,  65 
Trophoneuroses,  140,  151 
articular,  151 
muscular,  140 
of  bones,  151 
of  joints,  151 
of  teeth,  151 
osseous,  151 
visceral,  156 
Tubercular  meningitis,  653 

pathology  of,  667 
Tumors  of  the  brain,  632  • 
of  the  spinal  cord,  564 
Twelfth,  spasm  of,  371 


ULCP^K,  perforating,  147 
Ulnar  nerve,  disease  of,  396 
Unconsciousness,  135 
Unilateral  atrophy  of  the  brain,  477 
facial  paralysis,  365 
myelitis,  557 

pathology  of,  655 
treatment  of,  656 
oculo-moior  monoplegia,  504 
progressive  atrophy  of  the  face,  149 
myelitis,  560 
Urethral  neuralgia,  267 
Uterine  neuralgia,  265 


INDEX, 


723 


VAGUS,  diseases  of  the.  299,377 
Vaginismus,  266 
Vascular  diseases  of  the  brain,  G03 

of  the  spinal  membranes,  569 
spinal  sclerosis,  539 
Vaso-motor  functions,  66 

nervous  mechanism,  216 
disorders  of,  218 
Vertigo,  138,160 
aural,  509 
lab_yrin  thine,  509 
Vesicular  column  of  Clarke,  44 
Violin-players'  spasm,  310 
Visceral  angioneuroses,  219 
kinesioneuroses,  194 
neuralgia,  262 
paralgesia,  133 


Voluntary  movements,  159 
Vdluptnous  feelings,  excess  of,  133 


WALK,  hemiplegic,  478 
Walking,  78 
"Wallerian  degeneration,  iOO 
White  softening,  110 
Wrist  clonus,  177 
Writers'  cramp,  308 

morbid  anatomy  of,  345 
treatment  of,  351 
Wry-neck,  302 


YAWNING,  attacks  of,  311 
Yellow  softening,  110 


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